Publications by authors named "Xiaoquan Guo"

37 Publications

Preparation of the peroxisome proliferator-activated receptor α polyclonal antibody: Its application in fatty liver hemorrhagic syndrome.

Int J Biol Macromol 2021 Apr 7;182:179-186. Epub 2021 Apr 7.

Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China. Electronic address:

Peroxisome proliferator-activated receptor α (PPARα) play a key role in the regulation of metabolic homeostasis, inflammation, cellular growth, and differentiation. To further explore the potential role of PPARα in the energy homeostasis of fatty liver hemorrhagic syndrome (FLHS), we reported the prokaryotic expression and purification of chicken PPARα subunit protein, and successfully prepared a polyclonal antibody against PPARα recombinant protein. The 987 bp PPARα subunit genes were cloned into the pEASY-T3 clone vector. Then the plasmid PCR products encoding 329 amino acids were ligated to pEASY-Blunt E2 vector and transformed into BL21 to induce expression. The recombinant PPARα subunit protein, containing His-tag, was purified by affinity column chromatography using Ni-NTA affinity column. Rabbit antiserum was generated by using the concentration of recombinant PPARα subunit protein as the antigen. The results of western blotting showed that the antiserum can specifically recognize chicken endogenous PPARα protein. Immunohistochemistry and immunofluorescence showed that the PPARα mainly existed in the nucleus of hepatocytes, renal epithelial cells and hypothalamic endocrine nerve cells. More importantly, western blotting and real-time quantitative PCR indicated that FLHS significantly decreased the expression of PPARα.
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http://dx.doi.org/10.1016/j.ijbiomac.2021.04.018DOI Listing
April 2021

Serum Metabolomic Profiling to Reveal Potential Biomarkers for the Diagnosis of Fatty Liver Hemorrhagic Syndrome in Laying Hens.

Front Physiol 2021 9;12:590638. Epub 2021 Feb 9.

Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China.

Fatty liver hemorrhage syndrome (FLHS), a nutritional and metabolic disease that frequently occurs in laying hens, causes serious losses to the poultry industry. Nowadays, the traditional clinical diagnosis of FLHS still has its limitations. Therefore, searching for some metabolic biomarkers and elucidating the metabolic pathway are useful for the diagnosis and prevention of FLHS. In the present study, a model of FLHS in laying hens induced by feeding a high-energy, low-protein diet was established. Gas chromatography time-of-flight mass spectrometry (GC-TOF-MS) was used to analyze the metabolites in serum at days 40 and 80. The result showed that, in total, 40 differential metabolites closely related to the occurrence and development of FLHS were screened and identified, which were mainly associated with lipid metabolism, amino acid metabolism, and energy metabolism pathway disorders. Further investigation of differential metabolites showed 10 potential biomarkers such as 3-hydroxybutyric acid, oleic acid, palmitoleic acid, and glutamate were possessed of high diagnostic values by analyzing receiver operating characteristic (ROC) curves. In conclusion, this study showed that the metabolomic method based on GC-TOF-MS can be used in the clinical diagnosis of FLHS in laying hens and provide potential biomarkers for early risk evaluation of FLHS and further insights into FLHS development.
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http://dx.doi.org/10.3389/fphys.2021.590638DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7900428PMC
February 2021

Nephropathogenic Infectious Bronchitis Virus Infection Altered the Metabolome Profile and Immune Function of the Bursa of Fabricius in Chicken.

Front Vet Sci 2020 21;7:628270. Epub 2021 Jan 21.

Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China.

Infectious bronchitis is a highly contagious, acute viral respiratory disease of chickens, regardless of the strain, and its infection may lead to considerable economic losses to the poultry industry. New nephropathogenic infectious bronchitis virus (NIBV) strains have increasingly emerged in recent years; hence, evaluating their infection-influenced immune function changes and the alteration of metabolite profiling is important. Initially, chickens were randomly distributed into two groups: the control group (Con) and the disease group (Dis). Here, the partial cytokines were examined, and the metabolome alterations of the bursa of Fabricius (BF) in NIBV infections in chickens were profiled by gas chromatography time-of-flight/mass spectrometry (GC-TOF/MS). The results revealed that the NIBV infection promotes the mRNA expression of inflammatory cytokines. Metabolic profile analysis indicated that clustering differed between the two groups and there were 75 significantly different metabolites detected between the two groups, suggesting that the host metabolism was significantly changed by NIBV infection. Notably, the following 12 metabolites were identified as the potential biomarkers: 3-phenyllactic acid, 2-deoxytetronic acid, aminomalonic acid, malonamide 5, uric acid, arachidonic acid, 2-methylglutaric acid, linoleic acid, ethanolamine, stearic acid, N-alpha-acetyl-l-ornithine, and O-acetylserine. Furthermore, the results of the correlation analysis showed that a strong correlation existed between metabolic biomarkers and inflammatory cytokines. Our results describe an immune and metabolic profile for the BF of chickens when infected with NIBV and provide new biomarkers of NIBV infection as potential targets and indicators of indicating therapeutic efficacy.
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http://dx.doi.org/10.3389/fvets.2020.628270DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7858655PMC
January 2021

Dysregulated expression of mRNA and SNP in pulmonary artery remodeling in ascites syndrome in broilers.

Poult Sci 2021 Mar 28;100(3):100877. Epub 2020 Nov 28.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, School of Land Resources and Environment, Key Laboratory of Agricultural Resource and Ecology in the Poyang Lake Basin of Jiangxi Province, Jiangxi Agricultural University, Nanchang 330045, PR China. Electronic address:

Broiler ascites syndrome (AS), also called pulmonary artery hypertension, is a metabolic disorder that has been observed worldwide in fast-growing broilers. Pulmonary arterial remodeling is a key step in the development of AS. The precise relationship between mRNA and SNP of the pulmonary artery in regulating AS progression remains unclear. In this study, we obtained pulmonary artery tissues from broilers with AS to perform pathologic section and pathologic anatomic observation. SNP, InDel, and mRNA data analysis were carried out using GATK and ANNOVAR software to study the SNP loci of 985 previously reported genes (437 upregulated and 458 downregulated). The pathology results showed that there was a lot of yellow fluid in the abdominal cavity and pericardium, that the ascites cardiac index and hematocrit changed significantly, and that the pulmonary artery had remodeled and become thicker in the disease group. Myocardial sections showed vacuolar degeneration of myocytes and rupture of muscle fibers. In addition, ALDH7A1, IRG1, GGT5, IGSF1, DHX58, USP36, TREML2, SPAG1, CD34, and PLEKHA7 were found to be closely associated with the pathogenesis of pulmonary artery remodeling in AS progression. Taken together, our present study further illuminates the molecular mechanism of pulmonary artery remodeling underlying AS progression.
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http://dx.doi.org/10.1016/j.psj.2020.11.054DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7936122PMC
March 2021

Activation of AMP-activated protein kinase signaling pathway ameliorates steatosis in laying hen hepatocytes.

Poult Sci 2021 Mar 4;100(3):100805. Epub 2020 Nov 4.

Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China. Electronic address:

The fatty liver hemorrhage syndrome in laying hens is a disease of lipid metabolism disorders. Importantly, energy sensor AMP-activated protein kinase (AMPK) plays an essential role in homeostasis regulation of liver lipid. The current research aims to investigate the relationship between AMPK signaling pathway and lipid metabolism in laying hen hepatocytes and explore the underlying mechanisms. The steatotic hepatocytes model of laying hen was established and treated with AMPK agonist AICAR and inhibitor compound C. The results showed that the levels of triglyceride, total cholesterol, and low-density lipoprotein cholesterol significantly declined while high-density lipoprotein cholesterol level increased in the AICAR-treated steatosis group compared with the steatosis group. Furthermore, the mRNA levels of liver kinase B1 and AMP-activated protein kinase α1 declined significantly in the steatosis group compared with those in the normal group. However, AMPK activation significantly upregulated the mRNA levels of peroxisome proliferator-activated receptor α and carnitine palmitoyl transferase-1 while downregulated the mRNA levels of acetyl CoA carboxylase, fatty acid synthase, 3-hydroxy-3-methyl glutaryl coenzyme A reductase, Sn-glycerol-3-phosphate acyltransferase, and hepatocyte nuclear factor 4α. These results suggest that activated AMPK signaling pathway increases fatty acid oxidation and reduces lipid synthesis in laying hen hepatocytes, thereby ameliorating liver steatosis.
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http://dx.doi.org/10.1016/j.psj.2020.10.059DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7936166PMC
March 2021

Inhibition of ROS/NLRP3/Caspase-1 mediated pyroptosis attenuates cadmium-induced apoptosis in duck renal tubular epithelial cells.

Environ Pollut 2020 Oct 23;273:115919. Epub 2020 Oct 23.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang, 330045, Jiangxi, PR China. Electronic address:

Cadmium (Cd) is an occupational and environmental pollutant, which mainly causes nephrotoxicity by damaging renal proximal tubular cells. To evaluate the effects of Cd on pyroptosis and the relationship between pyroptosis and apoptosis in duck renal tubular epithelial cells, the cells were cultured with 3CdSO·8HO (0, 2.5, 5.0, or 10.0 μM Cd), N-acetyl-L-cysteine (NAC) (100.0 μM), Z-YVAD-FMK (10.0 μM) or the combination of Cd and NAC or Z-YVAD-FMK for 12 h, and then cytotoxicity was assessed. The results evidenced that Cd significantly increased the releases of interleukin-18 (IL-18) and interleukin-1β (IL-1β), lactate dehydrogenase (LDH) and nitric oxide (NO), relative conductivity and cellular reactive oxygen species (ROS) level. Simultaneously, Cd also markedly upregulated NLRP3, Caspase-1, ASC, NEK7, IL-1β and IL-18 mRNA levels and NLRP3, Caspase-1 p20, GSDMD and ASC protein levels. Additionally, NAC notably improved the changes of above indicators induced by Cd. Combined treatment with Cd and Z-YVAD-FMK remarkably elevated Bcl-2 mRNA and protein levels, inhibited p53, Bax, Bak-1, Cyt C, Caspase-9 and Caspase-3 mRNA levels and p53, Bax, Bak-1, Caspase-9/cleaved Caspase-9 and Caspase-3/cleaved Caspase-3 protein levels, increased mitochondrial membrane potential (MMP), decreased apoptosis ratio and cell damage compared to treatment with Cd alone. Taken together, Cd exposure induces duck renal tubular epithelial cell pyroptosis through ROS/NLRP3/Caspase-1 signaling pathway, and inhibiting Caspase-1 dependent pyroptosis attenuates Cd-induced apoptosis.
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http://dx.doi.org/10.1016/j.envpol.2020.115919DOI Listing
October 2020

Cloning and prokaryotic expression of the chicken liver kinase B1 (LKB1) and its localization in liver, heart and hypothalamus.

Int J Biol Macromol 2021 Feb 29;169:513-520. Epub 2020 Dec 29.

Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China. Electronic address:

Liver kinase B1 (LKB1) is a member of the serine/threonine kinase family, which plays an indispensable role in the organism of animals. In the current study, the chicken LKB1 protein gene was amplified by PCR based on the primers and cDNA templates. Then, the cloning vector was constructed and the target gene was cloned. After that, the target gene was inserted into the expression vector to construct the recombinant plasmid. The recombinant plasmid was transformed into BL21 (DE3) host cells and the LKB1 recombinant proteins were successfully expressed by using Isopropyl-β-D-thiogalactopyranoside (IPTG). Finally, purified LKB1 proteins were used as antigen and the rabbit-derived antiserums were collected. The antiserum titer determined by ELISA was not less than 1:128000. The results of Western blot suggested that the polyclonal antibody is highly specific to chicken LKB1 protein. Immunofluorescence indicated that the LKB1 protein is mainly expressed in the cytoplasm of liver, heart and hypothalamus cells of chicken. Our study showed that the LKB1 polyclonal antibodies produced by this method are effective and can be used to further study the role of LKB1 in the pathogenesis of chicken disease.
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http://dx.doi.org/10.1016/j.ijbiomac.2020.12.195DOI Listing
February 2021

Activation of the ROS/HO-1/NQO1 signaling pathway contributes to the copper-induced oxidative stress and autophagy in duck renal tubular epithelial cells.

Sci Total Environ 2021 Feb 26;757:143753. Epub 2020 Nov 26.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, Jiangxi, PR China. Electronic address:

The aim of this study was to investigate the crosstalk between oxidative stress and autophagy through the ROS/HO-1/NQO1 pathway caused by copper (Cu). Duck renal tubular epithelial cells were treated in Cu sulfate (CuSO) (0, 100 and 200 μM) for 12 h, and in the combination of CuSO (200 μM) and reactive oxygen species (ROS) scavenger (butyl hydroxyanisole, BHA, 100 μM), or HO-1 inhibitor (zinc protoporphyrin, ZnPP, 10 μM) for 12 h. Results revealed that Cu could significantly elevate the levels of intracellular ROS, superoxide dismutase, hydrogen peroxide, malondialdehyde, glutathione, simultaneously reduce catalase and glutathione peroxidase levels, and upregulate HO-1, SOD-1, CAT, NQO1, GCLM mRNA levels and HO-1, SOD-1 protein levels. Additionally, Cu could observably increase the number of autophagosomes, acidic vesicle organelles (AVOs) and LC3 puncta; upregulate mRNA levels of mTOR, Beclin-1, ATG7, ATG5, ATG3, LC3II and protein levels of Beclin-1, LC3II/LC3I, downregulate LC3I mRNA level. Both treatments with BHA and ZnPP could significantly alleviate the changes of antioxidant indexes levels and ROS accumulation, reduce the increase of the number of autophagosomes, AVOs and LC3 puncta, and mitigate the above changed oxidative stress and autophagy related mRNA and protein levels induced by Cu. In summary, our findings indicated that excessive Cu could induce oxidative stress and autophagy by activating the ROS/HO-1/NQO1 pathway, and inhibition of HO-1 might attenuate Cu-induced oxidative stress and autophagy in duck renal tubular epithelial cells.
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http://dx.doi.org/10.1016/j.scitotenv.2020.143753DOI Listing
February 2021

Endoplasmic reticulum stress aggravates copper-induced apoptosis via the PERK/ATF4/CHOP signaling pathway in duck renal tubular epithelial cells.

Environ Pollut 2021 Mar 2;272:115981. Epub 2020 Nov 2.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang, 330045, Jiangxi, PR China. Electronic address:

Copper (Cu) is a vital micronutrient required for numerous fundamental biological processes, but excessive Cu poses potential detrimental effects on public and ecosystem health. However, the molecular details linking endoplasmic reticulum (ER) stress and apoptosis in duck renal tubular epithelial cells have not been fully elucidated. In this study, duck renal tubular epithelial cells exposed to Cu sulfate (CuSO) (0, 100 and 200 μM) and a PERK inhibitor (GSK2606414, GSK, 1 μM) for 12 h were used to investigate the crosstalk between ER stress and apoptosis under Cu exposure. Cell and ER morphological and functional characteristics, intracellular calcium (Ca) levels, apoptotic rates, ER stress and apoptosis-related mRNA and protein levels were examined. The results showed that excessive Cu could cause ER expansion and swelling, increase the expression levels of ER stress-associated genes (PERK, eIF2α, ATF4 and CHOP) and proteins (p-PERK and CHOP), induce intracellular Ca overload, upregulate the expression levels of apoptosis-associated genes (Bax, Bak1, Caspase9 and Caspase3) and the cleaved-Caspase3 protein, downregulate Bcl-xl and Bcl2 mRNA levels and trigger apoptosis. PERK inhibitor treatment could ameliorate the above changed factors caused by Cu. In conclusion, these findings indicate that excessive Cu could trigger ER stress via activation of the PERK/ATF4/CHOP signaling pathway and that ER stress might aggravate Cu-induced apoptosis in duck renal tubular epithelial cells.
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http://dx.doi.org/10.1016/j.envpol.2020.115981DOI Listing
March 2021

Exposed to Mercury-Induced Oxidative Stress, Changes of Intestinal Microflora, and Association between them in Mice.

Biol Trace Elem Res 2021 May 30;199(5):1900-1907. Epub 2020 Jul 30.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.

Twelve Kunming mice were randomly divided into two groups (n = 6), and administered with distilled water containing 0 mg/L and 160 mg/L HgCl respectively, with an experimental period of 3 days. Our results showed that mercury exposure significantly reduced weight gain in mice (P < 0.01). Through pathological observation of cecum tissues, significant pathological changes were observed in cecum tissues of mice exposed to mercury. Furthermore, mercury exposure not only significantly increased malondialdehyde (MDA) content in mice (P < 0.01) but also significantly decreased superoxide dismutase (SOD) activity (P < 0.01) and glutathione peroxidase (GSH) level in mice (P < 0.01). Furthermore, high-throughput sequencing analysis showed that at the genus level some microbial populations including Clostridiales, Lactobacillus, Treponema, Oscillospira, and Desulfovibrio were significantly increased whereas some microbial populations including S24-7, Acinetobacter, and Staphylococcus were significantly decreased. Moreover, correlation analysis indicated that microorganisms were not correlated with biomarkers of oxidative stress. In summary, mercury exposure reduced the growth performance of mice, resulting in gut microbiota alterations, and led to oxidative stress by increasing the concentration of malondialdehyde (MDA) and decreasing the concentration of superoxide dismutase (SOD) and glutathione peroxidase (GSH).
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http://dx.doi.org/10.1007/s12011-020-02300-xDOI Listing
May 2021

Subchronic oral mercury caused intestinal injury and changed gut microbiota in mice.

Sci Total Environ 2020 Jun 29;721:137639. Epub 2020 Feb 29.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China. Electronic address:

Mercury is a key global pollutant, yet the mechanism by which mercury-exposure causes intestinal injury is not clear, we aimed to investigate the mechanism of intestinal injury and gut microbiota changes caused by mercury-exposure. Twelve Kunming mice were divided into two groups (n = 6), and the two groups were treated with 0 mg/L and 80 mg/L HgCl in drinking water for 90 days respectively. Our results showed that mercury-exposure prominently effected body weight gain and glucose levels. The mercury-exposed mice showed intestinal injury, which was diagnosed by Histopathological Examination and Transmission Electron Microscopy. Meanwhile, RT-PCR indicated that mercury-exposure significantly increased the expression of pro-apoptotic genes including Bax, JNK, ASK1, caspase3 and TNF-α, and significantly decreased the expression of the anti-apoptotic gene Bcl-2. Furthermore, high-throughput sequencing analysis showed that at the genus level some microbial populations including Coprococcus, Oscillospira and Helicobacter were significantly increased whereas some microbial populations including Lgnatzschineria, Salinicoccus and Bacillus were significantly decreased. Moreover, PICRUSt analysis revealed potential metabolic changes. Correlation analysis indicated that microorganisms were significantly correlated with apoptotic gene expression. In summary, our results indicated that mercury-exposure affected the growth and development of mice, induced intestinal microbiota dysbiosis and metabolic disorder, and aggravated apoptosis in mice.
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http://dx.doi.org/10.1016/j.scitotenv.2020.137639DOI Listing
June 2020

Investigation of the effects of dichlorvos poisoning on AMPK signaling pathway in chicken brain tissues.

Environ Pollut 2020 Jun 12;261:114109. Epub 2020 Feb 12.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China. Electronic address:

Dichlorvos is a common crop insecticide widely used by people which causes extensive and serious environmental pollution. However, it has been shown that organophosphorus poisoning causes energy metabolism and neural disorders. The overall purpose of this study was to investigate the damage to brain tissue and the changes in AMPK signaling pathway-related gene expression after dichlorvos poisoning in chickens. White-feathered broiler chickens, as the research subjects of this experiment, were divided into three groups: control group, low-dose group (77.5% dichlorvos at 1.13 mg/kg dose) and high-dose group (77.5% dichlorvos at 10.2 mg/kg dose). Clinical symptoms were observed after modeling, and an integrative analysis was conducted using HE staining microscopy, immune-histochemical microscopy, electron microscopy and PCR arrays. The results showed that the high-dose group had more obvious dyspnea, salivation, convulsion and other neurological phenomena. Pathological sections showed that nuclear disintegration of neurons was most obvious in the low-dose group, and apoptosis of brain cells was most obvious in the high-dose group, and the mitochondrial structure was destroyed in the two poisoned group, i.e. low-dose group and high-dose group. PCR arrays showed that AMPK signaling pathway was inhibited and the expressions of genes involved in energy metabolism (ACACA and PRKAA1) were significantly changed. Furthermore, genes associated with protein synthesis (EIF4EBP1) were significantly upregulated. FASN and HMGCR expressions were significantly increased. There were significant changes in the expressions of cell cycle-related genes (STK11, TP53 and FOXO3). Organophosphate poisoning can cause a lot of nuclear disintegration of brain neurons, increases cell apoptosis, disrupts the energy metabolism of mitochondrial structure, and inhibits the AMPK signaling pathway. These results provide a certain idea and basis for studying the mechanism of AMPK signaling after organophosphorus poisoning and provide a research basis for the prevention and treatment of organophosphorus poisoning.
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http://dx.doi.org/10.1016/j.envpol.2020.114109DOI Listing
June 2020

16S rRNA gene sequencing reveals an altered composition of the gut microbiota in chickens infected with a nephropathogenic infectious bronchitis virus.

Sci Rep 2020 02 26;10(1):3556. Epub 2020 Feb 26.

Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.

Infectious bronchitis virus (IBV), a member of the Coronaviridae family, causes serious losses to the poultry industry. Intestinal microbiota play an important role in chicken health and contribute to the defence against colonization by invading pathogens. The aim of this study was to investigate the link between the intestinal microbiome and nephropathogenic IBV (NIBV) infection. Initially, chickens were randomly distributed into 2 groups: the normal group (INC) and the infected group (IIBV). The ilea were collected for morphological assessment, and the ileal contents were collected for 16S rRNA gene sequencing analysis. The results of the IIBV group analyses showed a significant decrease in the ratio of villus height to crypt depth (P < 0.05), while the goblet cells increased compared to those in the INC group. Furthermore, the microbial diversity in the ilea decreased and overrepresentation of Enterobacteriaceae and underrepresentation of Chloroplast and Clostridia was found in the NIBV-infected chickens. In conclusion, these results showed that the significant separation of the two groups and the characterization of the gut microbiome profiles of the chickens with NIBV infection may provide valuable information and promising biomarkers for the diagnosis of this disease.
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http://dx.doi.org/10.1038/s41598-020-60564-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7044311PMC
February 2020

A Multi-Omics Study of Chicken Infected by Nephropathogenic Infectious Bronchitis Virus.

Viruses 2019 11 16;11(11). Epub 2019 Nov 16.

Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, China.

Chicken gout resulting from nephropathogenic infectious bronchitis virus (NIBV) has become a serious kidney disease problem in chicken worldwide with alterations of the metabolic phenotypes in multiple metabolic pathways. To investigate the mechanisms in chicken responding to NIBV infection, we examined the global transcriptomic and metabolomic profiles of the chicken's kidney using RNA-seq and GC-TOF/MS, respectively. Furthermore, we analyzed the alterations in cecal microorganism composition in chickens using 16S rRNA-seq. Integrated analysis of these three phenotypic datasets further managed to create correlations between the altered kidney transcriptomes and metabolome, and between kidney metabolome and gut microbiome. We found that 2868 genes and 160 metabolites were deferentially expressed or accumulated in the kidney during NIBV infection processes. These genes and metabolites were linked to NIBV-infection related processes, including immune response, signal transduction, peroxisome, purine, and amino acid metabolism. In addition, the comprehensive correlations between the kidney metabolome and cecal microbial community showed contributions of gut microbiota in the progression of NIBV-infection. Taken together, our research comprehensively describes the host responses during NIBV infection and provides new clues for further dissection of specific gene functions, metabolite affections, and the role of gut microbiota during chicken gout.
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http://dx.doi.org/10.3390/v11111070DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893681PMC
November 2019

Effects of subchronic exposure of mercuric chloride on intestinal histology and microbiota in the cecum of chicken.

Ecotoxicol Environ Saf 2020 Jan 13;188:109920. Epub 2019 Nov 13.

Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China. Electronic address:

This study aimed to investigate the influences of mercuric chloride (HgCl, 250 ppm, drink water) on the growth performance, cecal morphology and microbiota of chickens (n = 60) after 30, 60, and 90 days of exposure. A control group of sixty chickens received water free of HgCl. Our results suggested that mercury exposure reduced the body weight and changed the cecal morphology of chickens after the 90-day treatment. Furthermore, sequence analysis of 16 S rRNA gene revealed that the diversity and composition of cecal microbiota in chickens differed between the control and exposure group. At the phylum level, Proteobacteria and Tenericutes phyla both significantly increased in mercury exposure groups on day 30 while only Tenericutes phyla significantly increased on day 60. At the genus level, we observed that the change in microbial populations are most dramatic on day 30. Besides, compared with the control group, the genus Prevotellaceae_UCG-001 significantly increased in exposure group on day 30 but showed no significant difference on day 60, whereas there was a significant decrease on day 90. PICRUSt analysis revealed potential metabolic changes, such as Bacterial invasion of epithelial cells and Metabolism of xenobiotics, associated with mercury exposure in chickens. Taken together, the data show that subchronic exposure to mercury not only affected the growth and development but also caused the dysbiosis of gut microbiota, which may further induced metabolic disorders in chickens.
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http://dx.doi.org/10.1016/j.ecoenv.2019.109920DOI Listing
January 2020

Insulin resistance and metabonomics analysis of fatty liver haemorrhagic syndrome in laying hens induced by a high-energy low-protein diet.

Sci Rep 2019 07 12;9(1):10141. Epub 2019 Jul 12.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang, 330045, Jiangxi, P.R. China.

Fatty liver haemorrhagic syndrome (FLHS) is a widespread metabolic disease in laying hens that causes a decrease in egg production and even death. Insulin resistance is a major contributor to the pathogenesis of nonalcoholic fatty liver disease. However, the relationship between FLHS and the insulin resistance mechanisms underlying FLHS is not well elucidated. Therefore, we established an FLHS model induced by feeding a high-energy low-protein diet. In the current study, we found that the fasting glucose and insulin concentrations were elevated in the FLHS group compared with the control group during the experimental period. The results of the oral glucose tolerance test (OGTT) and insulin sensitivity test (IST) showed a high level of insulin resistance in the FLHS model. InsR, 4EBP-1, Glut-1 and Glut-3 mRNA expression were decreased, and TOR, S6K1, and FOXO1 were elevated (P < 0.05). Metabolomic analysis with GC/MS identified 46 differentially expressed metabolites between these two groups, and of these, 14 kinds of metabolism molecules and 32 kinds of small metabolism molecules were decreased (P < 0.05). Further investigation showed that glucose, lipid and amino acid metabolism blocks in the progression of FLHS by GO functional and pathway analysis. Overall, these results suggest that insulin resistance participated in FLHS; comprehensively, metabolites participated in the dysregulated biological process.
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http://dx.doi.org/10.1038/s41598-019-46183-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6626135PMC
July 2019

Copper Changes Intestinal Microbiota of the Cecum and Rectum in Female Mice by 16S rRNA Gene Sequencing.

Biol Trace Elem Res 2020 Feb 30;193(2):445-455. Epub 2019 May 30.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang, 330045, Jiangxi, People's Republic of China.

The aim of the present study was to investigate the effects of high concentrations of copper (Cu) on the cecum and rectum of intestinal microbiota in female mice. Twenty-four Kunming mice were weighed and randomly divided into two groups (n = 12 per group) including the control group and Cu group. Cu group was given drinking water with 5 mg/kg-bw copper chloride (CuCl), while the control group was treated with drinking water without CuCl. At the 90th day, results showed that compared with the control group, mice in the treatment group had a lower body weight, and the feces turned yellow and had a lower pH value. Histopathological lesions showed that the intestinal tissue from the treatment group had increased thickness of outer muscularis and smoothed muscle fiber, widened submucosa, decreased goblet cells, and showed blunting of intestinal villi and severe atrophy of central lacteal. In addition, at the genus level, 16S rRNA gene sequencing from the Cu group showed that Corynebacterium were significantly increased whereas Staphylococcaceae, Odoribacter, Rikenella, and Jeotgalicoccus were significantly decreased in the cecum. Dehalobacterium, Coprococcus, and Spirochaetales increased significantly whereas Salinicoccus, Bacillales, Staphylococcus, and Lactobacillales decreased sharply in the rectum. This study demonstrated that high concentrations of Cu could induce tissue injury and interrupt the homeostasis of microbiota.
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http://dx.doi.org/10.1007/s12011-019-01718-2DOI Listing
February 2020

Effects of fatty liver hemorrhagic syndrome on the AMP-activated protein kinase signaling pathway in laying hens.

Poult Sci 2019 May;98(5):2201-2210

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, Jiangxi, P. R. China.

In mammals, the AMP-activated protein kinase (AMPK) pathways in the central and peripheral tissues coordinately integrate inputs from multiple sources to regulate energy balance. To investigate the effects of the fatty liver hemorrhagic syndrome (FLHS) caused by high-energy, low-protein diets and to explore the potential role of AMPK in the energy homeostasis of FLHS, 60 laying hens were equally divided into 2 groups: control group (basal diet) and experimental group (high-energy, low-protein diet). Liver tissues were subjected to histopathological analysis. Liver tissues were also collected on the 100th day to determine the levels of total cholesterol, triglyceride (TG), high-density lipoprotein cholesterol (HDL-Ch), low-density lipoprotein cholesterol (LDL-Ch), aspartate aminotransferase, and alanine aminotransferase in plasma. Additionally, the mRNA expression levels of AMPK signaling pathway related genes in liver were determined by quantitative RT-PCR. The results showed that histopathological lesions presented different degrees of lipid vacuolization in hepatocytes. In combination with hematoxylin and eosin and oil red O staining, the experimental group was divided into mild group and severe group. In the severe group, contents of TG and LDL-Ch were extremely significantly increased (P < 0.01) compared to the control group, and HDL-Ch content was extremely significantly decreased (P < 0.01). The serine-threonine kinase 11 and AMPKα1 mRNA expression levels were downregulated, while acetyl-CoA carboxylase, fatty acid synthase, hepatocyte nuclear factor-4α, 3-hydroxy-3-methyl glutaryl coenzyme A reductase and carnitine palmitoyltransferase-I mRNA expression levels were upregulated by a high-energy and low-protein diet. Taken together, these findings suggest that a functional AMPK signaling pathway exists in chickens and AMPK may alter the energy balance in the FLHS induced by high-energy, low-protein diets.
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http://dx.doi.org/10.3382/ps/pey586DOI Listing
May 2019

High Doses of Copper and Mercury Changed Cecal Microbiota in Female Mice.

Biol Trace Elem Res 2019 May 13;189(1):134-144. Epub 2018 Aug 13.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health Economic and Technological Development District, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Nanchang, 330045, Jiangxi, People's Republic of China.

The aim of the present study was to investigate the effects of high doses of copper (Cu) and mercury (Hg) on the cecal microbiota in female mice. Forty-eight Kunming mice were randomly divided into the control group (CCk group), the Cu group (CCu group), the Hg group (CHg group), and the Cu + Hg group (CCH group). At the 90th day, cecal tissues were prepared for histopathological analysis and cecal contents for analysis by 16S rRNA sequencing method. Cecal tissues from treatment groups had histopathological lesions including increased thickness of inner muscularis and outer muscularis, widened submucosa, decreased goblet cells, mild to moderate necrosis of enterocytes, blunting of intestinal villi, and severe atrophy of central lacteal. Furthermore, compared to the CCk group, the abundance of bacteria genera Rikenella, Jeotgailcoccus, and Staphylococcus were significantly decreased, whereas the bacteria genus Corynebacterium was significantly increased in the CCu group. The abundance of bacteria genera of Sporosarcina, Jeotgailcoccus, and Staphylococcus were significantly decreased in the CHg group and CCH group. The bacteria genus Anaeroplasma was significantly increased in the CCH group. The results indicated that high doses of Cu and Hg caused histopathological lesions and changed the diversity of microbiota in the cecum of female mice, which provide a theoretical basis for more accurate assessment of the risk in intestinal diseases caused by Cu and Hg.
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http://dx.doi.org/10.1007/s12011-018-1456-1DOI Listing
May 2019

Alterations of mitochondrial antioxidant indexes and apoptosis in duck livers caused by Molybdenum or/and cadmium.

Chemosphere 2018 Feb 14;193:574-580. Epub 2017 Nov 14.

Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, Jiangxi, PR China. Electronic address:

Cadmium (Cd) and high Molybdenum (Mo) can lead to adverse reactions on animals, but the co-induced toxicity of Mo and Cd to liver in ducks was not well understood. To investigate the co-induced toxic effects of Mo combined with Cd on mitochondrial oxidative stress and apoptosis in duck livers. 240 healthy 11-day-old ducks were randomly divided into 6 groups (control, LMo group, HMo group, Cd group, LMoCd group and HMoCd group). After being treated for 30, 60, 90 and 120 days, liver mitochondrial antioxidant indexes, ceruloplasmin (CP), metallothionein (MT), Bak-1 and Caspase-3 genes mRNA expression levels, and ultrastructural changes were evaluated. The results showed that total antioxidative capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD) and xanthine oxidase (XOD) activities in experimental groups were decreased, whereas malondialdehyde (MDA) content and nitric oxide synthase (NOS) activity were increased compared with control group, and these changes of co-treated groups were more obvious in the later period of the experiment. The mRNA expression levels of CP, Bak-1 and Caspase-3 were up-regulated in experimental groups compared with control group and showed significant difference between co-treated groups and single treated groups. The mRNA expression level of MT in Cd group was higher than that in co-treated groups. Additionally, ultrastructural changes showed karyopyknosis, mitochondrial swelling, vacuolation and disruption of mitochondrial cristae in co-treated groups. Taken together, it was suggested that dietary Mo and Cd might lead to mitochondrial oxidative stress and apoptosis in duck livers, and it showed a possible synergistic relationship between the two elements.
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http://dx.doi.org/10.1016/j.chemosphere.2017.11.063DOI Listing
February 2018

The relationship between liver-kidney impairment and viral load after nephropathogenic infectious bronchitis virus infection in embryonic chickens.

Poult Sci 2017 Jun;96(6):1589-1597

To examine the relationship of impairments of the liver and kidney with viral load after nephropathogenic infectious bronchitis virus (NIBV) infection in embryonic chickens, 120 specific-pathogen-free Leghorn embryonated chicken eggs were randomly divided into two groups (infected and control), with three replicates per group and 20 eggs in each replicate. The eggs in the infected and control groups were challenged with 0.2 mL of 105.5 ELD50 NIBV and sterile saline solution, respectively. The embryonic chickens' plasma and liver and kidney tissues were collected at 1, 3, and 5 days post-inoculation (dpi), the liver and kidney functional parameters were quantified, and the tissue viral loads were determined with real-time PCR. The results showed that plasma potassium, sodium, chlorine, magnesium, calcium, and phosphorus levels were increased. The infected group exhibited significantly higher plasma uric acid, blood urea nitrogen, and creatinine levels than the control group at 3 dpi. The plasma concentrations of aspartate aminotransferase and alanine aminotransferase were significantly increased in the infected group. The total protein, albumin, and globulin levels in the infected group were significantly lower than those in the control group. The liver-kidney viral load in the infected group peaked at 3 dpi, at which time the kidney viral load was significantly higher than that of the liver. Our results indicated that NIBV infection caused liver and kidney damage in the embryonic chickens, and the results also demonstrated that the liver and kidney damage was strongly related to the tissue viral load following NIBV infection in embryonic chickens.
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http://dx.doi.org/10.3382/ps/pew455DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7107109PMC
June 2017

Dysregulated expression of microRNAs and mRNAs in pulmonary artery remodeling in ascites syndrome in broiler chickens.

Oncotarget 2017 Jan;8(2):1993-2007

Institute of Animal Population Health, College of Animal Science and Technology, JiangXi Agricultural University, Zhimin, Nanchang Economic and Technological Development District, Nanchang, P.R. China.

Ascites syndrome (AS), also known as pulmonary artery hypertension, remains a challenging disease that severely affects both humans and broiler chickens. Pulmonary artery remodeling presents a key step in the development of AS. In this study, we obtained pulmonary artery tissues from broilers with and without AS to perform miRNA sequencing analysis, miRNA-mRNA association analysis and pathological examinations. 29 significantly differentially expressed miRNAs were found both in known and novel miRNAs with 18 up-regulated and 11 down-regulated miRNAs. Their predicted potential targets were involved in a wide range of functional clusters as indicated via GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) analyses. The upregulation of miR-155, miR-23b-3p, miR-146b-5p and miR-146b-3p were found closely associated with the pathogenesis of pulmonary artery remodeling in AS progression. The association analysis for the miRNAs-mRNAs showed that these 29 significantly differentially expressed miRNAs regulate 162 differentially expressed target genes. Among them, 20 miRNAs correlated with 18 predicted target genes that appear to be involved in pulmonary artery remodeling, mainly in three broad physiological processes: the hypoxia sensing response (HIF1α, NHE1, STAT5 and STAT3), endothelial permeability dysfunction (CD44, TRAF2, CDK2AP1, LZTFL1, JAZF1, PEBP1, LRP1B, RPS14 and THBS2) and inflammation (MEOX2, STAT5, STAT3, IRF8, MAP3K8, IL-1BETA and TNFRSF1B). Pathological pulmonary artery remodeling in the AS broilers was consistently observed in the present study. Taken together, the current analysis further illuminates the molecular mechanism of pulmonary artery remodeling underlying AS progression.
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http://dx.doi.org/10.18632/oncotarget.12888DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356772PMC
January 2017

Telocytes in pancreas of the Chinese giant salamander (Andrias davidianus).

J Cell Mol Med 2016 11 20;20(11):2215-2219. Epub 2016 Sep 20.

College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China.

Telocytes (TCs), novel interstitial cells, have been identified in various organs of many mammals. However, information about TCs of lower animals remains rare. Herein, pancreatic TCs of the Chinese giant salamanders (Andrias davidianus) were identified by CD34 immunohistochemistry (IHC) and transmission electron microscopy (TEM). The IHC micrographs revealed CD34 TCs with long telopodes (Tps) that were located in the interstitium of the pancreas. CD34 TCs/Tps were frequently observed between exocrine acinar cells and were close to blood vessels. The TEM micrographs also showed the existence of TCs in the interstitium of the pancreas. TCs had distinctive ultrastructural features, such as one to three very long and thin Tps with podoms and podomers, caveolae, dichotomous branching, neighbouring exosomes and vesicles. The Tps and exosomes were found in close proximity to exocrine acinar cells and α cells. It is suggested that TCs may play a role in the regeneration of acinar cells and α cells. In conclusion, our results demonstrated the presence of TCs in the pancreas of the Chinese giant salamander. This finding will assist us in a better understanding of TCs functions in the amphibian pancreas.
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http://dx.doi.org/10.1111/jcmm.12948DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082396PMC
November 2016

Tanshinone IIA protects against pulmonary arterial hypertension in broilers.

Poult Sci 2017 May;96(5):1132-1138

This investigation was conducted to study the effects of tanshinone IIA (TIIA) on pulmonary arterial hypertension (PAH) in broilers. Two-hundred newly hatched Arbor Acre commercial broilers were randomly divided into 3 groups. All groups, with the exception of the control group (tap water), were given NaCl water (0.3%) starting on the d 15, and broilers in the protected group were fed a diet supplemented with TIIA (2.5 g/kg) starting on the d 15. On d 28, 35, 42, and 49, the ratio of the right ventricular weight to the total ventricular weight (RV: TV) and the values of other biochemical indicators for each group chickens were determined. The concentrations of interleukin-6 (IL-6), interleukin-1β (IL-1β), nuclear factor kappa (NF-κB), and P38 (a mitogen-activated protein kinase) were measured using enzyme-linked immune sorbent assays (ELISA). The results showed that the proportion of chickens in the diseased group with an RV:TV ratio in the range of 0.250 to 0.299 (10%) was significantly higher (25 to 30%) compared to that of the other groups (P < 0.05), and the proportion in all chickens was 28%. In addition, the IL-6, IL-1β, NF-κB, and P38 protein concentrations were higher in the diseased group, whereas there were no differences between the control group and the protected group. Moreover, the measurements of body weight, liver function, kidney function and electrolytes showed significant differences between the diseased group and the other groups. These findings suggest that tanshinone IIA may protect broilers from PAH, which is an important piece of information for the poultry industry.
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http://dx.doi.org/10.3382/ps/pew322DOI Listing
May 2017

Telocytes in gastric lamina propria of the Chinese giant salamander, Andrias davidianus.

Sci Rep 2016 09 15;6:33554. Epub 2016 Sep 15.

College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China.

In this study, we attempt to identify gastric telocytes (TCs) of the Chinese giant salamander Andrias davidianus, by light microscopy, immunohistochemistry and transmission electron microscopy (TEM) methods. Toluidine blue staining showed TCs with one to two very thin and long telopodes (Tps) that were located in gastric lamina propria. Tps had characteristic structures, including podoms, podomers and dichotomous branching. Immunohistochemistry showed the existence of CD34(+)/PDGFRα(+) TCs with moniliform Tps in stroma and were close to gastric glands and blood vessels. TEM micrographs also demonstrated the presence of TCs in interstitium between gastric glands. TCs/Tps were located in close proximity to gastric glands, blood vessels, endocrine cells and stem cells. In particular, Tps frequently surrounded stem cells. TCs and Tps, Tps and stem cells established close contacts. Moreover, the exosomes were also found near TCs/Tps. Our data confirmed the presence of TCs in gastric lamina propria of the amphibian, and suggested that TCs cooperate with resident stem cells to regulate endocrine cells and gastric glands regeneration and homeostasis.
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http://dx.doi.org/10.1038/srep33554DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5024317PMC
September 2016

The co-induced effects of molybdenum and cadmium on the mRNA expression of inflammatory cytokines and trace element contents in duck kidneys.

Ecotoxicol Environ Saf 2016 Nov 21;133:157-63. Epub 2016 Jul 21.

Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agriculture University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, Jiangxi, PR China. Electronic address:

The aims of this study were determining the co-induced effects of dietary Cadmium (Cd) and high intake of Molybdenum (Mo) on renal toxicity in ducks. 240 healthy 11-day-old ducks were randomly divided into 6 groups, which were treated with Mo or/and Cd at different doses added to the basal diet for 120 days. Ducks of control group were fed with basal diet, LMo and HMo groups were fed with 15mg/kg Mo and 100mg/kg Mo respectively; ducks of Cd group were provided with 4mg/kg Cd which was added into basal diet. Two combination groups were treated with 15mg/kg Mo+4mg/kg Cd and 100mg/kg Mo+4mg/kg Cd respectively. On days 30, 60, 90 and 120, the mRNA expression levels of inflammatory cytokines and contents of trace elements were detected. In addition, transmission electron microscopic examination was used for ultrastructural studies. The results indicated that the mRNA expression levels of tumor necrosis factor-α (TNF-α), nuclear factor-kappa B (NF-κB), and cyclooxygenase-2 (COX-2) showed an upward tendency in treatment groups in comparison with control group, and in the later period of the experiment it showed a significant rise in joint groups compared with the Mo and Cd group (P<0.01); the contents of copper (Cu) and iron (Fe) decreased in joint groups in the later period (P<0.05) while the contents of Mo and Cd significantly increased (P<0.01); zinc (Zn) and selenium (Se) concentration had a slight downtrend in treated groups, but showed no significant difference (P>0.05). The ultrastructural analysis showed that kidney tissues were severely injured in joint groups on day 120. These results suggested that the combination of Mo and Cd could aggravate damages to the kidney. In addition, dietary of Mo or/and Cd caused the decrease of Cu, Fe, Zn, and Se contents, inflammatory response and pathological lesions whose mechanism is somehow linked with Mo and Cd deposition in kidney.
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http://dx.doi.org/10.1016/j.ecoenv.2016.07.007DOI Listing
November 2016

Transcriptome Analysis and Gene Identification in the Pulmonary Artery of Broilers with Ascites Syndrome.

PLoS One 2016 8;11(6):e0156045. Epub 2016 Jun 8.

Institute of Animal Population Health, College of Animal Science and Technology, JiangXi Agriculture University, N.O. 1101, Zhimin Avenue, Nanchang Economic and Technological Development District Nanchang, 330045, P. R. China.

Background: Pulmonary arterial hypertension, also known as Ascites syndrome (AS), remains a clinically challenging disease with a large impact on both humans and broiler chickens. Pulmonary arterial remodeling presents a key step in the development of AS. The precise molecular mechanism of pulmonary artery remodeling regulating AS progression remains unclear.

Methodology/principal Findings: We obtained pulmonary arteries from two positive AS and two normal broilers for RNA sequencing (RNA-seq) analysis and pathological observation. RNA-seq analysis revealed a total of 895 significantly differentially expressed genes (DEGs) with 437 up-regulated and 458 down-regulated genes, which were significantly enriched to 12 GO (Gene Ontology) terms and 4 KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways (Padj<0.05) regulating pulmonary artery remodeling and consequently occurrence of AS. These GO terms and pathways include ribosome, Jak-STAT and NOD-like receptor signaling pathways which regulate pulmonary artery remodeling through vascular smooth cell proliferation, inflammation and vascular smooth cell proliferation together. Some notable DEGs within these pathways included downregulation of genes like RPL 5, 7, 8, 9, 14; upregulation of genes such as IL-6, K60, STAT3, STAT5 Pim1 and SOCS3; IKKα, IkB, P38, five cytokines IL-6, IL8, IL-1β, IL-18, and MIP-1β. Six important regulators of pulmonary artery vascular remodeling and construction like CYP1B1, ALDH7A1, MYLK, CAMK4, BMP7 and INOS were upregulated in the pulmonary artery of AS broilers. The pathology results showed that the pulmonary artery had remodeled and become thicker in the disease group.

Conclusions/significance: Our present data suggested some specific components of the complex molecular circuitry regulating pulmonary arterial remodeling underlying AS progression in broilers. We revealed some valuable candidate genes and pathways that involved in pulmonary artery remodeling further contributing to the AS progression.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0156045PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4898705PMC
July 2017

Prokaryotic expression of the chicken xanthine oxidase (XOD) subunit and its localization in liver and kidney.

Int J Biol Macromol 2016 Jun 4;87:341-7. Epub 2016 Mar 4.

Clinical Veterinary Laboratory, College of Animal Science and Technology, Jiangxi Agricultural University, Jiangxi, China.

Xanthine oxidase (XOD) is the members of the molybdenum hydroxylase flavoprotein family and it plays a vital role in the body's purine catabolism. In this study, we cloned the XOD 37kDa subunit protein by using RT-PCR and pMD-18-T clone vector based on the total RNA extracted from chicken liver. The cloning XOD subunit protein gene was ligated into the pET-32a to construct the recombinant plasmid pET-XOD. After the pET-XOD expression vector was transformed into host cells Rosetta (DE3), the recombinant XOD subunit proteins (54.8kDa) were successfully induced by isopropy1 β-d-thiogalactoside (IPTG). Rabbit antiserums were produced by using the purification of the recombinant XOD subunit protein as antigen. The titer of the antiserum was more than 1:102,400 determined by using ELISA. The result of Western blot demonstrated that the antiserum could specifically recognize the chicken liver XOD. Immunohistochemistry and immunofluorescence showed that the XOD mainly presented in the cytoplasm of chicken hepatocytes and proximal tubular epithelial cells. Our results indicated that the XOD subunit protein polyclonal antibody prepared by this method could be used for the further researches of the biological function of the XOD in the chicken.
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http://dx.doi.org/10.1016/j.ijbiomac.2016.03.001DOI Listing
June 2016

Oxidative Stress and Cell Apoptosis in Caprine Liver Induced by Molybdenum and Cadmium in Combination.

Biol Trace Elem Res 2016 Sep 16;173(1):79-86. Epub 2016 Feb 16.

Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agriculture University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang, 330045, Jiangxi, People's Republic of China.

To investigate the effects of co-exposure to molybdenum (Mo) and cadmium (Cd) on oxidative stress and cell apoptosis in caprine livers, 36 Boer goats were randomly divided into four groups with nine goats in each group. Three groups were randomly assigned with one of three oral treatments of CdCl2 (0.5 mg Cd kg(-1)·BW) and [(NH4)6Mo7O24·4H2O] (15 mg Mo kg(-1)·BW, 30 mg Mo kg(-1)·BW, 45 mg Mo kg(-1)·BW), while the control group received deionized water. Liver tissues on days 0, 25, and 50 were subjected to determine antioxidant activity indexes and the messenger RNA (mRNA) expression levels of ceruloplasmin (CP), cysteinyl aspartate-specific proteinase-3 (caspase-3), second mitochondria-derived activator of caspases (Smac), and cytochrome-C (Cyt-C) genes. The results showed that significant reductions were observed in total antioxidant capacity (T-AOC) and total superoxide dismutase (T-SOD) activities (P < 0.05), while activities or contents of malondialdehyde (MDA), nitric oxide (NO), and nitric oxide synthase (NOS) were increased (P < 0.05). The mRNA expression levels of CP, caspase-3, Smac, and Cyt-C genes were upregulated (P < 0.05). In addition, histopathological lesions showed different degrees of vacuolar degeneration and edematous and mitochondrial swelling. The results suggest that co-exposure to Mo and Cd could induce oxidative stress and cell apoptosis possibly associated with mitochondrial intrinsic pathway in goat liver and show possible synergistic effects between the two elements.
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http://dx.doi.org/10.1007/s12011-016-0633-3DOI Listing
September 2016

Telocytes in ileum of the Chinese giant salamander: ultrastructural evidence.

J Cell Mol Med 2016 Mar 25;20(3):568-74. Epub 2016 Jan 25.

College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China.

Telocytes (TCs) and their telopodes (Tps) have been found in various organs of many mammals, including in lower animals. However, knowledge of TCs in lower animals is still very limited. This study identified TCs and their Tps in the ileum of the Chinese giant salamander, Andrias davidianus (Amphibia: Caudata), by transmission electron microscopy. The TCs/Tps were found near epithelial cells, glandular cells and unmyelinated nerve fibres. Moreover, exosomes were also found to be present in between TCs/Tps and these cells.
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http://dx.doi.org/10.1111/jcmm.12741DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759476PMC
March 2016