Publications by authors named "Guyue Li"

25 Publications

  • Page 1 of 1

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

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

Inhibition of autophagy aggravates molybdenum-induced mitochondrial dysfunction by aggravating oxidative stress in duck renal tubular epithelial cells.

Ecotoxicol Environ Saf 2021 Feb 18;209:111771. Epub 2020 Dec 18.

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:

Excessive molybdenum (Mo) has adverse effects on animals. To elucidate the effects of autophagy on Mo-induced nephrotoxicity, the duck renal tubular epithelial cells were cultured in medium in absence and presence of (NH)MoO.4HO (0, 480, 720, 960 μM Mo), 3-Methyladenine (3-MA) (2.5 μM), and the combination of Mo and 3-MA for 12 h. After 12 h exposure, the MDC staining, morphologic observation, LC3 puncta, cell viability, autophagy-related genes mRNA and proteins levels, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) level, antioxidant indices, mitochondrial membrane potential (MMP), mitochondrial mass, mitochondrial respiratory control ratio (RCR) and oxidative phosphorylation rate (OPR) were determined. The results showed that excessive Mo exposure significantly elevated the number of autophagosome and LC3 puncta, upregulated Beclin-1, Atg5, LC3A and LC3B mRNA levels, and LC3II/LC3I and Beclin-1 protein levels, decreased mTOR, p62 and Dynein mRNA levels and p62 protein level. Besides, co-treatment with Mo and 3-MA dramatically increased LDH release, ROS level, hydrogen peroxide (HO) and malondialdehyde (MDA) contents as well as cell dam age, reduced cell viability, the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), MMP, mitochondrial mass, mitochondrial RCR and OPR compared to treatment with Mo alone. Taken together, these results suggest that excessive Mo exposure can induce autophagy in duck renal tubular epithelial cells, inhibition of autophagy aggravates Mo-induced mitochondrial dysfunction by regulating oxidative stress.
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http://dx.doi.org/10.1016/j.ecoenv.2020.111771DOI 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

Cadmium and molybdenum co-exposure triggers autophagy via CYP450s/ROS pathway in duck renal tubular epithelial cells.

Sci Total Environ 2021 Mar 11;759:143570. Epub 2020 Nov 11.

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

Cadmium (Cd) and excessive molybdenum (Mo) are detrimental to animals, but the combined nephrotoxic impacts of Cd and Mo on duck are still unclear. To evaluate the combined impacts of Cd and Mo on autophagy via Cytochrome P450s (CYP450s)/reactive oxygen species (ROS) pathway, duck renal tubular epithelial cells were treated with 3CdSO·8HO (4.0 μM Cd), (NH)MoO·4HO (500.0 μM Mo), butylated hydroxy anisole (BHA) (100.0 μM) and combination of Cd and Mo or Cd, Mo and BHA for 12 h, and combined cytotoxicity was investigated. The results indicated that Mo or/and Cd induced CYP1A1, CYP1B1, CYP2C9, CYP3A8 and CYP4B1 mRNA levels, decreased superoxide dismutase (SOD), catalase (CAT) activities and glutathione peroxidase (GSH-Px) content, and increased malondialdehyde (MDA) and hydrogen peroxide (HO) contents. Besides, Mo or/and Cd elevated the number of autophagosome and microtubule-associated protein light chain 3 (LC3) puncta, upregulated mRNA levels of Beclin-1, LC3A, LC3B, Atg5 and adenosine 5'-monophosphate (AMP)-activated protein kinase α1 (AMPKα-1), inhibited Dynein, p62 and mammalian target of rapamycin (mTOR) mRNA levels, increased Beclin-1 and LC3II/LC3I protein levels. Moreover, the changes of these factors in Mo and Cd co-treated groups were more apparent. Additionally, BHA could efficiently alleviate the changes of above these indicators co-induced by Mo and Cd. Overall, these results manifest Cd and Mo co-exposure may synergistically trigger autophagy via CYP450s/ROS pathway in duck renal tubular epithelial cells.
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http://dx.doi.org/10.1016/j.scitotenv.2020.143570DOI Listing
March 2021

Inhibition of autophagy enhances cadmium-induced apoptosis in duck renal tubular epithelial cells.

Ecotoxicol Environ Saf 2020 Dec 21;205:111188. Epub 2020 Aug 21.

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:

Increasing evidence indicates autophagy and apoptosis are involved in the toxicity mechanism of heavy metals. Our previous studies showed that cadmium (Cd) could induce autophagy and apoptosis in duck kidneys in vivo, nevertheless, the interaction between them has yet to be elucidated. Herein, the cells were either treated with 3CdSO·8HO (0, 1.25, 2.5, 5.0 μM Cd) or/and 3-methyladenine (3-MA) (2.5 μM) for 12 h and the indictors related autophagy and apoptosis were detected to assess the correlation between autophagy and apoptosis induced by Cd in duck renal tubular epithelial cells. The results demonstrated that Cd exposure notably elevated intracellular and extracellular Cd contents, the number of autophagosomes and LC3 puncta, up-regulated LC3A, LC3B, Beclin-1, Atg5 mRNA levels, and Beclin-1 and LC3II/LC3I protein levels, down-regulated mTOR, p62 and Dynein mRNA levels and p62 protein level. Additionally, autophagy inhibitor 3-MA decreased Beclin-1, LC3II/LC3I protein levels and increased p62 protein level. Moreover, co-treatment with Cd and 3-MA could notably elevate Caspase-3, Cyt C, Bax, and Bak-1 mRNA levels, Caspase-3 and cleaved Caspase-3 protein levels, and cell apoptotic rate as well as cell damage, decreased mitochondrial membrane potential (MMP), Bcl-2 mRNA level and the ratio of Bcl-2 to Bax compared to treatment with Cd alone. Overall, these results indicate Cd exposure can induce autophagy in duck renal tubular epithelial cells, and inhibition of autophagy might aggravate Cd-induced apoptosis through mitochondria-mediated pathway.
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http://dx.doi.org/10.1016/j.ecoenv.2020.111188DOI Listing
December 2020

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

Corrigendum to: Developmental competence of mature yak vitrified-warmed oocytes is enhanced by IGF-I via modulation of CIRP during in vitro maturation [Cryobiol. 71(3) (2015) 493-498].

Cryobiology 2020 02 19;92:281. Epub 2020 Jan 19.

Gansu Province Livestock Embryo Engineering Research Center, College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, China. Electronic address:

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http://dx.doi.org/10.1016/j.cryobiol.2020.01.007DOI Listing
February 2020

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

Abnormal expression of liver autophagy and apoptosis-related mRNA in fatty liver haemorrhagic syndrome and improvement function of resveratrol in laying hens.

Avian Pathol 2020 Apr 7;49(2):171-178. Epub 2020 Jan 7.

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

Fatty liver haemorrhagic syndrome (FLHS) is characterized by hepatic rupture and haemorrhage leading to sudden death in laying hens. Resveratrol (Res) is a natural polyphenol with antioxidant and anti-inflammatory effects that can ameliorate chronic liver disease. The aim of this study was to investigate the improved effect of Res on the altered expression of autophagy and apoptosis-related genes in laying hens with FLHS. A total of 144 healthy 150-day-old laying hens were randomly divided into four groups: control group (standard diet), HELP group (high-energy-low-protein (HELP) diet), HELP + Res group (HELP diet with 400 mg/kg Res) and Res group (standard diet with 400 mg/kg Res). Histopathological lesions of the liver and the mRNA levels of Beclin-1, Atg5, Atg7, p62, Bcl-2, Bax and Caspase-3 on days 40, 80, and 120 were measured. The results showed that lipid accumulation and hepatocyte damage in the HELP group were more serious than those in the HELP + Res group. The mRNA levels of Beclin-1, Atg5, Atg7, and Bcl-2 in the HELP and HELP + Res groups were strikingly declined (< 0.01) compared to the control group, and their mRNA levels were markedly higher in HELP group than those in the HELP + Res group (< 0.05). Additionally, the mRNA levels of p62, Bax and Caspase-3 were significantly increased in the HELP and HELP + Res groups (< 0.01 or < 0.05), but their mRNA levels in the HELP group were higher than those in the HELP + Res group (< 0.05). Collectively, FLHS could induce severe lipid accumulation, abnormal mRNA levels of liver autophagy and apoptosis-related genes. Res as a dietary supplement could attenuate these abnormal changes.
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http://dx.doi.org/10.1080/03079457.2019.1698712DOI Listing
April 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

A Hybrid Information Reconciliation Method for Physical Layer Key Generation.

Entropy (Basel) 2019 Jul 14;21(7). Epub 2019 Jul 14.

School of Cyber Science and Engineer, Southeast University, Nanjing 210096, China.

Physical layer key generation (PKG) has become a research focus as it solves the key distribution problem, which is difficult in traditional cryptographic mechanisms. Information reconciliation is a critical process in PKG to obtain symmetric keys. Various reconciliation schemes have been proposed, including the error detection protocol-based approach (EDPA) and error correction code-based approach (ECCA). Both EDPA and ECCA have advantages and drawbacks, regarding information leakage, interaction delay, and computation complexity. In this paper, we choose the BBBSS protocol from EDPA and BCH code from ECCA as a case study, analyzing their comprehensive efficiency performance versus pass number and bit disagreement ratio (BDR), respectively. Next, we integrate the strength of the two to design a new hybrid information reconciliation protocol (HIRP). The design of HIRP consists of three main phases, i.e., training, table lookup, and testing. To comprehensively evaluate the reconciliation schemes, we propose a novel efficiency metric to achieve a balance of corrected bits, information leakage, time delay, and computation time, which represents the effectively corrected bits per unit time. The simulation results show that our proposed method outperforms other reconciliation schemes to improve the comprehensive reconciliation efficiency. The average improvement in efficiency is 2.48 and 22.36 times over the BBBSS and BCH code, respectively, when the range of the BDR is from 0.5% to 11.5%. Compared to the BBBSS protocol and the BCH code, HIRP lies at a mid-level in terms of information leakage and computation time cost. Besides, with the lowest time delay cost, HIRP reaches the highest reconciliation efficiency.
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http://dx.doi.org/10.3390/e21070688DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7515191PMC
July 2019

Physical Layer Key Generation in 5G and Beyond Wireless Communications: Challenges and Opportunities.

Entropy (Basel) 2019 May 15;21(5). Epub 2019 May 15.

School of Cyber Science and Engineering, Southeast University, Nanjing 210096, China.

The fifth generation (5G) and beyond wireless communications will transform many exciting applications and trigger massive data connections with private, confidential, and sensitive information. The security of wireless communications is conventionally established by cryptographic schemes and protocols in which the secret key distribution is one of the essential primitives. However, traditional cryptography-based key distribution protocols might be challenged in the 5G and beyond communications because of special features such as device-to-device and heterogeneous communications, and ultra-low latency requirements. Channel reciprocity-based key generation (CRKG) is an emerging physical layer-based technique to establish secret keys between devices. This article reviews CRKG when the 5G and beyond networks employ three candidate technologies: duplex modes, massive multiple-input multiple-output (MIMO) and mmWave communications. We identify the opportunities and challenges for CRKG and provide corresponding solutions. To further demonstrate the feasibility of CRKG in practical communication systems, we overview existing prototypes with different IoT protocols and examine their performance in real-world environments. This article shows the feasibility and promising performances of CRKG with the potential to be commercialized.
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http://dx.doi.org/10.3390/e21050497DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7514987PMC
May 2019

Ascorbate-conjugated nanoparticles for promoted oral delivery of therapeutic drugs via sodium-dependent vitamin C transporter 1 (SVCT1).

Artif Cells Nanomed Biotechnol 2018;46(sup1):198-208. Epub 2017 Dec 20.

a Department of Pharmacy , the First Affiliated Hospital of China Medical University , Shenyang , China.

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http://dx.doi.org/10.1080/21691401.2017.1417864DOI Listing
August 2019

Colony-stimulating factor 2 enhances the developmental competence of yak (Poephagus grunniens) preimplantation embryos by modulating the expression of heat shock protein 70 kDa 1A.

Theriogenology 2017 Apr 23;93:16-23. Epub 2017 Jan 23.

Gansu Province Livestock Embryo Engineering Research Center, College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, China. Electronic address:

Colony-stimulating factor 2 (CSF) is known to promote the development and survival of rodents and ruminants preimplantation embryos; however, the effect of CSF on yak embryos has not been reported. The objective of this study was to investigate the effects of CSF on the developmental competence of yak embryos cultured in vitro in modified synthetic oviduct fluid (mSOF) medium and on the expression pattern of heat shock protein 70 kDa 1A (HSPA1A). In each experiment, cumulus-oocyte complexes (COCs) were matured in vitro and fertilized with frozen-thawed semen. Zygotes were treated with varying concentrations of CSF (0, 10, 50, 100 ng/mL) until day 8 after fertilization. Embryo development was calculated as the percentage of oocytes that formed embryos at the 2-cell, 4-cell, 8-cell, 16-cell, morula and blastocyst stages. The total cell numbers (TCN) per blastocyst and their allocation to the inner cell mass (ICM) and trophectoderm (TE) lineages were determined using differential CDX2 staining. The expression of HSPA1A was examined by quantitative real-time PCR (qRT-PCR) and immunochemistry to determine the mRNA and protein levels. The results showed that treatment with 50 ng/mL CSF significantly (P < 0.05) increased the rate of blastocyst formation (19.01% versus 9.93%) and the TCN per blastocyst (96.94 versus 81.41) compared to the control group. However, no significant differences were observed in the other stages of development. qRT-PCR analysis confirmed that treatment with 50 ng/mL CSF significantly (P < 0.05) inhibited the expression of HSPA1A mRNA in blastocysts cultured in vitro relative to the control group, but there were no significant differences between the other treatment groups. Immunocytochemical analysis confirmed that HSPA1A protein accumulation was gradually reduced in yak blastocysts cultured in 0, 10, 100 or 50 ng/mL CSF, however, no significant differences were observed between the 10 and 100 ng/mL treatments (P > 0.05). In conclusion, these findings demonstrate that CSF inhibits the expression of HSPA1A to facilitate yak blastocyst formation and increase cell numbers.
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http://dx.doi.org/10.1016/j.theriogenology.2017.01.034DOI Listing
April 2017

Developmental competence of mature yak vitrified-warmed oocytes is enhanced by IGF-I via modulation of CIRP during in vitro maturation.

Cryobiology 2015 Dec 27;71(3):493-8. Epub 2015 Oct 27.

Gansu Province Livestock Embryo Engineering Research Center, College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, China. Electronic address:

The objective of this study was to investigate whether developmental competence of mature vitrified-warmed yak (Bos grunniens) oocytes can be enhanced by supplemented insulin-like growth factor I (IGF-1) during in vitro maturation (IVM), and its relationship with the expression of cold-inducible RNA-binding protein (CIRP). In experiment 1, immature yak oocytes were divided into four groups, and IVM supplemented with 0, 50, 100 and 200 ng/mL IGF-1 was evaluated; the mRNA and protein expression levels of CIRP in mature oocytes in the four groups were evaluated using quantitative real-time PCR and western blotting analyses. In experiment 2, the mature yak oocytes in the four groups were cryopreserved using the Cryotop (CT) method, followed by chemical activation and in vitro culture for two days and eight days to determine cleavage, blastocyst rates, and total cell number in the blastocysts. Mature yak oocytes without vitrification served as a control group. The outcomes were as following: (1) the expression of CIRP in the matured oocytes was up-regulated in the IGF-1 groups and was highest expression was observed in the 100 ng/mL IGF-1 treatment group. (2) In the vitrified-warmed groups, the rates of cleavage and blastocyst were also highest in the 100 ng/mL IGF-1 treatment group (81.04 ± 1.06%% and 32.16 ± 1.01%), which were close to the rates observed in groups without vitrification (83.25 ± 0.85% and 32.54 ± 0.34%). The rates of cleavage and blastocyst in the other vitrified-warmed groups were 70.92 ± 1.32% and 27.33 ± 1.31% (0 ng/mL); 72.73 ± 0.74% and 29.41 ± 0.84% (50 ng/mL); 72.43 ± 0.61% and 27.61 ± 0.59% (200 ng/mL), respectively. There was no significant difference in the total cell number per blastocysts between the vitrified-warmed groups and group without vitrification. Thus, we conclude that the enhancement in developmental competence of mature yak vitrified-warmed oocytes after the addition of IGF-1 during IVM might result from the regulation of CIRP expression in mature yak oocytes prior to vitrification.
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http://dx.doi.org/10.1016/j.cryobiol.2015.10.150DOI Listing
December 2015

Insulinlike growth factor I improves yak (Bos grunniens) spermatozoa motility and the oocyte cleavage rate by modulating the expression of Bax and Bcl-2.

Theriogenology 2015 Sep 14;84(5):756-62. Epub 2015 May 14.

Gansu Province Livestock Embryo Engineering Research Center, College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, China. Electronic address:

The aim of our present study was to examine the effects of insulinlike growth factor 1 (IGF-1) on yak sperm motility during in vitro capacitation and the relationship between the effects of IGF-1 on yak sperm motility and apoptosis was evaluated. Frozen-thawed yak spermatozoa were incubated at 38 °C for 1 hour in Tyrode's bicarbonate-buffered medium for sperm culture (Sp-TALP) with different concentrations (0, 50, 100, and 200 ng/mL) of IGF-1. In every treatment, the sperm motility was measured by a computer-assisted sperm analyzer system. The fertilizing ability of spermatozoa was evaluated on the basis of oocyte cleavage rate after insemination. The expression of Bax and Bcl-2 was examined by real-time polymerase chain reaction and Western blot for the messenger RNA and protein levels. It is interesting to note that IGF-1 improved yak spermatozoa motility and the cleavage rate of oocytes; these improvements were highest in the 100 ng/mL IGF-1 group, followed by the 200 ng/mL and 50 ng/mL groups, with the lowest improvements in motility and cleavage rates in groups without IGF-1. The expression level of Bax was downregulated by IGF-1, whereas Bcl-2 was upregulated. Both messenger RNA and Bax proteins were lowest in groups with 100 ng/mL IGF-1, where the Bcl-2 was the highest. Bax expression in the groups with IGF-1 was lower than that in the group without IGF-1, and Bcl-2 expression was higher in groups with IGF-1 than that in the group without IGF-1. In conclusion, this research reports that improvements in yak spermatozoa motility and the oocyte cleavage rate after the addition of IGF-I may be a result of the reduction of spermatozoa apoptosis rates by modulating the expression of Bax and Bcl-2.
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http://dx.doi.org/10.1016/j.theriogenology.2015.05.007DOI Listing
September 2015

Association of heat shock protein 90 with the developmental competence of immature oocytes following Cryotop and solid surface vitrification in yaks (Bos grunniens).

Cryobiology 2015 Aug 3;71(1):33-9. Epub 2015 Jun 3.

Gansu Province Livestock Embryo Engineering Research Center, College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, China. Electronic address:

The correlation between the 90 kDa heat-shock protein (HSP90) and the developmental competence of yak (Bos grunniens) oocytes following the process of vitrification has not been studied clearly. In the present study, we compare the efficacies of Cryotop (CT) and solid surface vitrification (SSV) methods for the cryopreservation of immature yak oocytes. Yak cumulus oocyte complexes were randomly allocated into three groups: (1) controls, (2) CT vitrification, and (3) SSV vitrification. Oocytes were vitrified and in vitro maturated and fertilized. The percentages of nuclear maturation and in vitro development were evaluated. The vitrified-warmed oocytes were evaluated for mRNA and protein expression levels of HSP90 using quantitative real-time PCR and western blotting at various stages: matured oocytes, 2-8 cells embryos and blastocysts. No difference was found in the percentages of nuclear maturation, cleavage or blastocyst in the two vitrified groups; however, the rates of maturation were significantly lower than those in the control group. Among the three groups, the maturation rates in CT: 51.14±0.86% and SSV: 50.82±1.34% were less than those of the controls: 69.65±1.13%; the cleavage rates in CT: 39.16±1.01% and SSV: 39.08±0.92%, were less than those of the controls: 58.14±0.76%; but the blastocysts rates and total cell number in the blastocysts were similar: CT: 32.20±0.73% and 104.6±3.72; SSV: 32.35±0.81% and 102.4±1.34; and controls: 34.38±1.32% and 103.8±4.13, respectively. The HSP90 expression level in the matured oocytes and 2-8 cell embryos of the control group was significantly higher than that in the two vitrified groups; there was not significant difference in the blastocysts in the three groups. We thus conclude that CT and SSV perform equally in the vitrification of immature yak oocytes during the process of cryopreservation, and their influence on oocytes mainly occured from the maturation to cleavage stages. The HSP90 levels in the blastocysts of the vitrified groups increased is associated with the developmental competence of the embryo.
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http://dx.doi.org/10.1016/j.cryobiol.2015.06.005DOI Listing
August 2015