Publications by authors named "Feibo Xu"

19 Publications

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Polystyrene microplastics induce blood-testis barrier disruption regulated by the MAPK-Nrf2 signaling pathway in rats.

Environ Sci Pollut Res Int 2021 Apr 25. Epub 2021 Apr 25.

College of Basic Medicine & Xu Rongxiang Regenerative Medicine Research Center, Binzhou Medical University, Yantai, People's Republic of China.

As a persistent pollutant, microplastics (MPs) have been reported to induce sperm quantity decrease in mice. However, the related mechanism remains obscure. Therefore, this study is intended to explore the effects of polystyrene microplastics (PS-MPs) on male reproduction and its related mechanism of blood-testis barrier (BTB) impairment. Thirty-two adult male Wistar rats were divided randomly into four groups fed with PS-MPs for 90 days at doses of 0 mg/day (control group), 0.015 mg/day, 0.15 mg/day, and 1.5 mg/day, respectively. The present results have shown that PS-MP exposure led to the damage of seminiferous tubule, resulted in apoptosis of spermatogenic cells, and decreased the motility and concentration of sperm, while the abnormality of sperm was elevated. Meanwhile, PS-MPs could induce oxidative stress and activate the p38 MAPK pathway and thus deplete the nuclear factor erythroid-2 related factor 2 (Nrf2). Noteworthily, PS-MPs led to the BTB-related protein expression decrease. All these results demonstrated that PS-MP exposure may lead to the destruction of BTB integrity and the apoptosis of spermatogenic cells through the activation of the MAPK-Nrf2 pathway. The current study provided novelty evidence for elucidating the effects of PS-MPs on male reproductive toxicity and its potential mechanism.
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http://dx.doi.org/10.1007/s11356-021-13911-9DOI Listing
April 2021

AFB-induced mice liver injury involves mitochondrial dysfunction mediated by mitochondrial biogenesis inhibition.

Ecotoxicol Environ Saf 2021 Apr 7;216:112213. Epub 2021 Apr 7.

Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.

Aflatoxin B1 (AFB) pollutes foodstuffs and feeds, causing a food safety problem and seriously endangering human and animal health. Liver is the principal organ for AFB accumulation and biotransformation, during which AFB can cause acute and chronic liver damage, however, the specific mechanism is not completely clear. Mitochondria are the primary organelle of cellular bio-oxidation, providing 95% energy for liver to execute its multiple functions. Therefore, we speculated that mitochondrial dysfunction is involved in AFB-induced liver injury. To verify the hypothesis, a total of eighty healthy male mice were randomly divided into four groups on average, and exposed with 0, 0.375, 0.75 and 1.5 mg/kg body weight AFB by intragastric administration for 30 d. The results displayed that AFB triggered liver injury accompanied by oxidative stress. AFB exposure also damaged mitochondria structure, decreased mitochondrial membrane potential (MMP), as well as increased cytoplasmic cytochrome c (Cyt-c) protein expression, Bax, p53, Caspase-3/9 protein and/or mRNA expression levels and terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine-5'-triphosphate (dUTP) nick end labeling (TUNEL) staining positive cells in mice liver. Meanwhile, AFB exposure elevated pyruvate content, inhibited tricarboxylic acid (TCA) cycle rate-limiting enzymes and electron transport chain (ETC) complexes I-V activities, disturbed ETC complexes I-V subunits mRNA expression levels and reduced adenosine triphosphate (ATP) level in mice liver. These results indicated that AFB destroyed mitochondrial structure, activated mitochondrion-dependent apoptosis and induced mitochondrial dysfunction. In addition, AFB disrupted mitochondrial biogenesis, presented as the abnormalities of protein and/or gene expression levels of voltage dependent anion channel protein 1 (VDAC1), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor 1 (Nrf1) and mitochondrial transcription factor A (Tfam). This may contribute to hepatic and mitochondrial lesions induced by AFB. These results provide a new perspective for elucidating the mechanisms of AFB hepatotoxicity.
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http://dx.doi.org/10.1016/j.ecoenv.2021.112213DOI Listing
April 2021

Polystyrene microplastics cause granulosa cells apoptosis and fibrosis in ovary through oxidative stress in rats.

Toxicology 2021 02 24;449:152665. Epub 2020 Dec 24.

Department of Histology and Embryology, Binzhou Medical University, Yantai, PR China; College of Basic Medicine & Xu Rongxiang Regenerative Medicine Research Center, Binzhou Medical University, Yantai, PR China. Electronic address:

Microplastics (MPs) are receiving increased attention as a harmful environmental pollutant. Studies have investigated that MPs have reproductive toxicity, but the mechanism is little known. Here, we aimed to investigate the effects of polystyrene microplastics (PS-MPs) on ovary in rats and the underlying molecular mechanisms. in vivo, thirty-two female Wistar rats were exposed to 0.5 μm PS-MPs at different concentrations (0, 0.015, 0.15 and 1.5 mg/d) for 90 days. And then, all animals were sacrificed, ovaries and blood were collected for testing. in vitro, granulosa cells (GCs) were separated from rat ovary and treated with 0、1、5、25 μg/mL PS-MPs and reactive oxygen species (ROS) inhibitor N-Acetyl-l-cysteine (NAC) respectively. Our results showed that PS-MPs could enter into GCs and result in the reducing of growing follicles number. And the Enzyme-linked immunosorbent assay (ELISA) manifested that PS-MPs could obviously decrease the level of anti-Müllerian hormone (AMH). In addition, PS-MPs induced oxidative stress, apoptosis of GCs and ovary fibrosis evidenced by assay kits, flow cytometry, immunohistochemistry, Masson's trichrome and Sirius red staining. Moreover, the western blot assay manifested that PS-MPs exposure significantly increased the expression levels of Wnt/β-Catenin signaling pathways-related proteins (Wnt, β-catenin, p-β-catenin) and the main fibrosis markers (transforming growth factor-β (TGF-β), fibronectin, α-smooth muscle actin (α-SMA). Additionally, the expression levels of Wnt and p-β-catenin, apoptosis of GCs decreased after NAC treatment. In summary, polystyrene microplastics cause fibrosis via Wnt/β-Catenin signaling pathway activation and granulosa cells apoptosis of ovary through oxidative stress in rats, both of which ultimately resulted in decrease of ovarian reserve capacity.
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http://dx.doi.org/10.1016/j.tox.2020.152665DOI Listing
February 2021

Protective effects of lycopene against AFB-induced erythrocyte dysfunction and oxidative stress in mice.

Res Vet Sci 2020 Apr 13;129:103-108. Epub 2020 Jan 13.

Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. Electronic address:

To evaluate the protective role of lycopene (LYC) against aflatoxin B (AFB)-induced erythrocyte dysfunction and oxidative stress, male kunming mice were treated with LYC (5 mg/kg) and/or AFB (0.75 mg/kg) by intragastric administration for 30 d. Hematological indices were detected to assess erythrocyte function. The erythrocytes C3b receptor rate (E-C3bRR) and erythrocytes C3b immune complex rosette rate (E-ICRR) were detected to assess erythrocyte immune function. Hydrogen peroxide (HO) and malondialdehyde (MDA) contents and superoxide dismutase (SOD) and catalase (CAT) activities were determined to evaluate erythrocyte oxidative stress. The results showed that LYC administration significantly relieved AFB-induced erythrocyte dysfunction by increasing the levels of red blood cell count (RBC), hemoglobin (HGB) and hematocrit (HCT), as well as reducing red blood cell volume distribution width (RDW) level, while the levels of mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC) and mean platelet volume (MPV) had no significant differences among the four groups. Besides, LYC ameliorated AFB1-induced erythrocyte immune dysfunction by increasing E-C3bRR and decreasing E-ICRR. Furthermore, LYC also alleviated AFB-induced erythrocyte oxidative stress by decreasing HO and MDA contents and increasing SOD and CAT activities. These results indicated that LYC protected against AFB-induced erythrocyte dysfunction and oxidative stress in mice. The findings could lead a possible therapeutics for the management of AFB-induced erythrocyte toxicity.
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http://dx.doi.org/10.1016/j.rvsc.2020.01.015DOI Listing
April 2020

Iron Dyshomeostasis Participated in Rat Hippocampus Toxicity Caused by Aluminum Chloride.

Biol Trace Elem Res 2020 Oct 17;197(2):580-590. Epub 2019 Dec 17.

Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.

Aluminum (Al) alters iron regulatory factors content and leads to the changes in iron-related proteins causing iron accumulation. But limited evidence ascertains this hypothesis. Therefore, our experiment was conducted and four groups of male Wistar rats were orally administrated of 0, 50, 150, and 450 mg/kg BW/d aluminum chloride (AlCl) for 90 days by drinking water, respectively. The cognitive function, pathological lesion of hippocampus, oxidative stress, as well as iron-related proteins and iron regulatory factors expression were detected. The results showed that AlCl remarkably induced the oxidative stress and pathological lesion in the hippocampus and impaired the learning-memory ability. The contents of Al and iron increased in all AlCl-exposed groups. Meanwhile, the increased divalent metal transporter 1 (DMT1) expression enhanced iron import and the decreased ferroportin 1 (Fpn1) expression reduced iron export in AlCl-exposed groups. The iron accumulated and ferritin heavy chains (Fth) expression decreased in all AlCl-exposed groups led to an increase in free iron. The study also showed that iron regulatory factor iron regulatory protein 2 (IRP2) was decreased and hepcidin was increased in AlCl-exposed groups. The results indicated that AlCl induces iron dyshomeostasis presenting as iron accumulation, the disordered expression of iron import, export, store, and regulatory proteins in rat hippocampus accompanied with oxidative stress, pathological lesion, and impaired learning-memory ability.
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http://dx.doi.org/10.1007/s12011-019-02008-7DOI Listing
October 2020

Lycopene alleviates AFB-induced immunosuppression by inhibiting oxidative stress and apoptosis in the spleen of mice.

Food Funct 2019 Jul;10(7):3868-3879

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. and Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin 150030, China.

Lycopene (LYC) has been reported to exhibit antioxidant and immunoprotective activities, and our previous studies confirmed that LYC can alleviate multiple tissue damage induced by aflatoxin B1 (AFB1). However, it is unclear whether LYC could relieve the AFB1-induced immunosuppression. Thus, forty-eight male mice were randomly allocated and treated with LYC (5 mg kg-1) and/or AFB1 (0.75 mg kg-1) by intragastric administration for 30 days. We found that LYC alleviated AFB1-induced immunosuppression by relieving splenic structure injury and increasing the spleen weight, spleen coefficient, T lymphocyte subsets, the contents of IL-2, IFN-γ and TNF-α in serum, as well as the mRNA expression of IL-2, IFN-γ and TNF-α in spleen. Furthermore, LYC inhibited oxidative stress induced by AFB1via decreasing the levels of reactive oxygen species (ROS), hydrogen peroxide (H2O2) and malondialdehyde (MDA), while enhancing the total antioxidant capacity (T-AOC) and antioxidant enzyme activities. In addition, LYC also restrained splenic apoptosis through blocking mitochondria-mediated apoptosis in AFB1 intoxicated mice, presenting as the increase of mitochondrial membrane potential, and the decrease of cytoplasmic Cyt-c protein expression, cleaved Caspase-3 protein expression, Caspase-3/9 activities and mRNA expressions, as well as balancing the mitochondrial protein and mRNA expressions of Bax and Bcl-2. These results indicate that LYC can alleviate AFB1-induced immunosuppression by inhibiting oxidative stress and mitochondria-mediated apoptosis of mice spleen.
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http://dx.doi.org/10.1039/c8fo02300jDOI Listing
July 2019

Neuroprotective role of hyperforin on aluminum maltolate-induced oxidative damage and apoptosis in PC12 cells and SH-SY5Y cells.

Chem Biol Interact 2019 Feb 24;299:15-26. Epub 2018 Nov 24.

Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China. Electronic address:

Many reports demonstrated that aluminum maltolate (Almal) has potential toxicity to human and animal. Our study has demonstrated that Almal can induce oxidative damage and apoptosis in PC12 cells and SH-SY5Y Cells, two in vitro models of neuronal cells. Hyperforin (HF) is a well-known antioxidant, anti-inflammatory, anti-amyloid and anti-depressant compound extracted from Hypericum perforatum extract. Here, we investigated the neuroprotective effect of HF against Almal-induced neurotoxicity in cultured PC12 cells and SH-SY5Y cells, mainly caused by oxidative stress. In the present study, HF significantly inhibited the formation of reactive oxygen species (ROS), decreased the level of lipid peroxide and enhanced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) compared with Almal group in PC12 cells and SH-SY5Y cells. Additionally, HF suppressed the reduction of the mitochondrial membrane potential (MMP), cytochrome c (Cyt-c) release, activation of caspase-3, and the down-regulation of Bcl-2 expression and up-regulation of Bax expression induced by Almal in PC12 cells and SH-SY5Y cells. In summary, HF protects PC12 cells and SH-SY5Y cells from damage induced by Almal through reducing oxidative stress and preventing of mitochondrial-mediated apoptosis.
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http://dx.doi.org/10.1016/j.cbi.2018.11.016DOI Listing
February 2019

AlCl inhibits LPS-induced NLRP3 inflammasome activation and IL-1β production through suppressing NF-κB signaling pathway in murine peritoneal macrophages.

Chemosphere 2018 Oct 28;209:972-980. Epub 2018 Jun 28.

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin 150030, China. Electronic address:

Aluminum (Al), a common environmental pollutant, has been reported to inhibit the immune functions of macrophage. However, the mechanisms involved remain unclear. In this study, murine peritoneal macrophages were exposed to 0, 0.27, 0.54, and 1.08 mg/mL of aluminium chloride (AlCl) for 24 h, and then treated with 1 μg/mL lipopolysaccharide (LPS) for another 6 h. No addition of both AlCl and LPS serviced as control group. We observed that AlCl has cytotoxicity in murine peritoneal macrophages, showing a decrease in cell viability and an increase in lactate dehydrogenase release. Besides, AlCl exposure restrained the LPS-induced NLR pyrin domain containing 3 (NLRP3) inflammasome activation presented as NLRP3 expressions reduction, caspase-1 cleavage inhibition and interleukin 1 beta (IL-1β) maturation lessened. Meanwhile, AlCl exposure decreased LPS-induced IKKβ activity, IκBα phosphorylation, the phosphorylation and mRNA expression of NF-κB p65, as well the genes expression and concentration in medium supernatant of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6). The results suggested that AlCl inhibited the activation of NF-κB signaling pathway induced by LPS, which maybe one of the upstream signals involved in the inhibition of NLRP3 inflammasome activation by AlCl. This research can provide theoretical basis for understanding the immune toxicity of Al, and deepening the cognition of Al exposure hazards to immune response.
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http://dx.doi.org/10.1016/j.chemosphere.2018.06.171DOI Listing
October 2018

Aluminum trichloride-induced hippocampal inflammatory lesions are associated with IL-1β-activated IL-1 signaling pathway in developing rats.

Chemosphere 2018 Jul 27;203:170-178. Epub 2018 Mar 27.

Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. Electronic address:

Aluminum (Al) is a recognized environmental pollutant that causes neuroinflammatory lesions, leading to neurodegenerative diseases. Interleukin-1 (IL-1) signaling pathway is responsible for regulating inflammatory lesions. However, it remains unclear whether IL-1 signaling pathway is involved in neuroinflammatory lesions induced by Al exposure. In the present study, one hundred and twenty Wistar rats were orally exposed to 0, 50, 150 and 450 mg/kg BW/d aluminum trichloride (AlCl) for 90 days, respectively. We found that AlCl exposure increased hippocampal Al concentration, reduced hippocampus coefficient, impaired cognitive ability, deteriorated microstructure of hippocampal CA1 and CA3 regions, increased reactive oxygen species (ROS) level, activated astrocytes and microglia, increased pro-inflammatory cytokines contents and mRNA expressions, and decreased anti-inflammatory cytokines contents and mRNA expressions in the hippocampus. These results indicated that AlCl induced the hippocampal inflammatory lesion (HIL). Moreover, AlCl exposure increased the mRNA and protein expression of IL-1 signaling pathway core components in the hippocampus, demonstrating that AlCl activated IL-1 signaling pathway. Furthermore, the correlation between interleukin-1β (IL-1β) content and HIL and activation of the IL-1 signaling pathway was analyzed. Results showed that IL-1β content was positively correlated with pro-inflammatory cytokines contents and mRNA expressions and activation of IL-1 signaling pathway, and was negatively correlated with hippocampus coefficient, anti-inflammatory cytokines contents and mRNA expressions, and the number of hippocampal neurons. The above results demonstrate that AlCl-induced HIL is associated with IL-1 signaling pathway, in which IL-1β is a link.
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http://dx.doi.org/10.1016/j.chemosphere.2018.03.162DOI Listing
July 2018

Fas- and Mitochondria-Mediated Signaling Pathway Involved in Osteoblast Apoptosis Induced by AlCl.

Biol Trace Elem Res 2018 Jul 12;184(1):173-185. Epub 2017 Oct 12.

Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, No. 59 Mucai Street, Xiangfang District, Harbin, 150030, China.

Aluminum (Al) is known to induce apoptosis of osteoblasts (OBs). However, the mechanism is not yet established. To investigate the apoptotic mechanism of OBs induced by aluminum trichloride (AlCl), the primary OBs from the craniums of fetal Wistar rats were exposed to 0 mg/mL (control group, CG), 0.06 mg/mL (low-dose group, LG), 0.12 mg/mL (mid-dose group, MG), and 0.24 mg/mL (high-dose group, HG) AlCl for 24 h, respectively. We observed that AlCl induced OB apoptosis with the appearance of apoptotic morphology and increase of apoptosis rate. Additionally, AlCl treatment activated mitochondrial-mediated signaling pathway, accompanied by mitochondrial membrane potential (ΔΨm) depolarization, release of cytochrome c from the mitochondria to the cytoplasm, as well as survival signal-related factor caspase-9 and caspase-3 activation. AlCl exposure also activated Fas/Fas ligand signaling pathway, presented as Fas, Fas ligand, and Fas-associated death domain expression enhancement and caspase-8 activation, as well as the hydrolysis of Bid to truncated Bid, suggesting that the Fas-mediated signaling pathway might aggravate mitochondria-mediated OB apoptosis through hydrolyzing Bid. Furthermore, AlCl exposure inhibited Bcl-2 protein expression and increased the expressions of Bax, Bak, and Bim in varying degrees. These results indicated that AlCl exposure induced OB apoptosis through activating Fas- and mitochondria-mediated signaling pathway and disrupted B-cell lymphoma-2 family proteins.
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http://dx.doi.org/10.1007/s12011-017-1176-yDOI Listing
July 2018

Aluminum chloride caused liver dysfunction and mitochondrial energy metabolism disorder in rat.

J Inorg Biochem 2017 09 20;174:55-62. Epub 2017 Apr 20.

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. Electronic address:

Aluminum (Al) is known to exert hepatotoxicity. However, the mechanisms mostly are unclear. Liver is a metabolism organ that maintains the energy level and structural stability of body, mitochondria are the main sites of energy metabolism, thus, we hypothesized that mitochondrial energy metabolism disorder contributes to liver dysfunction in aluminum chloride (AlCl) treatment rat. To verify the hypothesis, forty male Wistar rats were randomly allocated and orally exposed to 0, 64mg/kg, 128mg/kg and 256mg/kg body weight AlCl in drinking water for 120days, respectively. We found that AlCl exposure reduced the electron transport chain complexes I-V activities and adenosine triphosphate (ATP) level, as well as disturbed mitochondrial DNA transcript, presenting as the inhibited mRNA expressions of NADH dehydrogenase 1, NADH dehydrogenase 2, cytochrome b, cytochrome c oxidase subunit 1, cytochrome c oxidase subunit 3 and ATP synthase 6, indicating that AlCl exposure disturbs the mitochondrial energy metabolism, and it caused an increase in liver enzymes (Aspartate aminotransferase and Alanine aminotransferase) and histopathological lesions. Additionally, we found that reactive oxygen species accumulation and decreased superoxide dismutase activity in mitochondria, and increased 8-Hydroxydeoxyguanosine levels in mitochondrial DNA, demonstrating AlCl exposure promotes mitochondrial oxidative stress, which may be a contributing factor to mitochondrial energy metabolism disorder and liver dysfunction. The study displayed that mitochondria are the potential target of liver damage induced by AlCl, providing considerable direction for the prevention and clinical intervention of liver diseases.
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http://dx.doi.org/10.1016/j.jinorgbio.2017.04.016DOI Listing
September 2017

Protective Effect of Selenium on Aflatoxin B1-Induced Testicular Toxicity in Mice.

Biol Trace Elem Res 2017 Dec 27;180(2):233-238. Epub 2017 Mar 27.

Institute of Special Animal and Plant Sciences of Chinese Academy of Agricultural Sciences, Changchun, 130112, China.

Aflatoxins have been considered as one of the major risk factors of male infertility, and aflatoxin B1 (AFB1) is the most highly toxic and prevalent member of the aflatoxins family. Selenium (Se), an essential nutritional trace mineral for normal testicular development and male fertility, has received extensive intensive on protective effects of male reproductive system due to its potential antioxidant and activating testosterone synthesis. To investigate the protective effect of Se on AFB1-induced testicular toxicity, the mice were orally administered with AFB1 (0.75 mg/kg) and Se (0.2 mg/kg or 0.4 mg/kg) for 45 days. We found that that Se elevated testes index, sperm functional parameters (concentration, malformation, and motility), and the level of serum testosterone in AFB1-exposed mice. Moreover, our results showed that Se attenuated the AFB1-induced oxidative stress and the reduction of testicular testosterone synthesis enzyme protein expression such as steroidogenic acute regulatory protein (StAR), P450 side-chain cleavage (P450scc), and 17β-hydroxysteroid dehydrogenase (17β-HSD) in AFB1-exposed mice. These results demonstrated that Se conferred protection against AFB1-induced testicular toxicity and can be attributed to its antioxidant and increased testosterone level by stimulating protein expression of StAR and testosterone synthetic enzymes.
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http://dx.doi.org/10.1007/s12011-017-0997-zDOI Listing
December 2017

The suppressive effects of aluminum chloride on the osteoblasts function.

Environ Toxicol Pharmacol 2016 Dec 18;48:125-129. Epub 2016 Oct 18.

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. Electronic address:

Aluminum (Al) exposure impairs bone formation, and bone formation is mediated by the osteoblasts. But effects of Al on the osteoblasts function remain elusive. The osteoblasts were exposed to 0, 0.0252, 0.126, 0.252mg/mL AlCl·6HO for 24h. The osteoblasts viability, TGF-β, BMP-2, IGF-I and Cbfα1 mRNA expressions, and GSH-P and SOD activities, ROS concentration were determined. The osteoblasts ultrastructural features were also observed. The results showed that AlCl suppressed the osteoblasts viability, TGF-β, BMP-2, IGF-I and Cbfα1 mRNA expressions, GSH-P and SOD activities, and elevated ROS concentration compared with the CG. The ultrastructural features of osteoblasts in the HG showed mitochondrial swelling, foam-like structure, uneven distribution of chromatin, incomplete cell membrane and cytoplasm spillover compared with the CG. It indicates that AlCl inhibits osteoblasts viability, growth regulation factors mRNA expressions, anti-oxidative function, and damaged the osteoblasts histology structure, impairing the osteoblasts function.
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http://dx.doi.org/10.1016/j.etap.2016.10.009DOI Listing
December 2016

Effects of Corticosterone on Immune Functions of Cultured Rat Splenic Lymphocytes Exposed to Aluminum Trichloride.

Biol Trace Elem Res 2016 Oct 23;173(2):399-404. Epub 2016 Mar 23.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.

Aluminum (Al) exposure is toxic to immune system. Studies have implicated that glucocorticoids (GCs) exert the dual regulation effect on the immune function depending on the concentration. However, it is unknown whether a dual effect of GCs exists in the AlCl3-treated lymphocytes. Corticosterone (Cort) is one kind of GCs. To investigate the effect of different concentration Cort on AlCl3-treated lymphocytes, rat splenic lymphocyte was isolated and cultured with 0.55 mmol/L AlCl3, simultaneously administrated Cort at final concentration of 0 (control group, CG), 10(-8) (low-level group, LG), and 10(-6) (high-level group, HG) mol/L, respectively. Another group without AlCl3 and Cort served as the blank group (BG). We found that low concentration Cort increased the T and B lymphocyte proliferation rate, proportions of CD4(+) T lymphocyte subset, IgG, IL-2, and TNF-α contents, whereas high concentration Cort decreased those in AlCl3-treated lymphocytes. In conclusion, the results of this study indicated that low concentration Cort relieves the immunotoxicity of AlCl3 on the splenic lymphocytes, whereas high concentration Cort aggravates it.
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http://dx.doi.org/10.1007/s12011-016-0678-3DOI Listing
October 2016

Aluminum chloride induces neuroinflammation, loss of neuronal dendritic spine and cognition impairment in developing rat.

Chemosphere 2016 May 15;151:289-95. Epub 2016 Mar 15.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China. Electronic address:

Aluminum (Al) is present in the daily life of humans, and the incidence of Al contamination increased in recent years. Long-term excessive Al intake induces neuroinflammation and cognition impairment. Neuroinflammation alter density of dendritic spine, which, in turn, influence cognition function. However, it is unknown whether increased neuroinflammation is associated with altered density of dendritic spine in Al-treated rats. In the present study, AlCl3 was orally administrated to rat at 50, 150 and 450 mg/kg for 90d. We examined the effects of AlCl3 on the cognition function, density of dendritic spine in hippocampus of CA1 and DG region and the mRNA levels of IL-1β, IL-6, TNF-α, MHC II, CX3CL1 and BNDF in developing rat. These results showed exposure to AlCl3 lead to increased mRNA levels of IL-1β, IL-6, TNF-α and MCH II, decreased mRNA levels of CX3CL1 and BDNF, decreased density of dendritic spine and impaired learning and memory in developing rat. Our results suggest AlCl3 can induce neuroinflammation that may result in loss of spine, and thereby leads to learning and memory deficits.
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http://dx.doi.org/10.1016/j.chemosphere.2016.02.092DOI Listing
May 2016

The Toxicity of Aluminum Chloride on Kidney of Rats.

Biol Trace Elem Res 2016 Oct 24;173(2):339-44. Epub 2016 Feb 24.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.

This study investigated the toxicity of aluminum chloride (AlCl3) exposure in the rat kidney. Forty male Wistar rats (5 weeks old), weighing 110-120 g, were randomly divided into four groups: control group (CG, 0 g/L AlCl3), low dose group (LG, 0.4 g/L AlCl3), mid dose group (MG, 0.8 g/L AlCl3), and high dose group (HG, 1.6 g/L AlCl3). Rats were administered AlCl3 in their drinking water for 120 days. A variety of measurements were taken including superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities, malondialdehyde (MDA) concentration in the kidney and blood urea nitrogen (BUN), and cystatin C (Cys-C) concentrations in the serum. In addition, Al and β2-microglobulin (β2-MG) concentrations and the activity of N-acetyl-β-D-glucosaminidase (NAG) in the urine were determined. The results showed that in the AlCl3-treated groups SOD and GSH-PX activities were decreased, while NAG activity and Al, MDA, BUN, Cys-C, and β2-MG concentrations were increased, compared with the CG. This study indicates that AlCl3 exposure induces oxidative stress and suppresses kidney function.
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http://dx.doi.org/10.1007/s12011-016-0648-9DOI Listing
October 2016

Aluminum trichloride inhibits osteoblastic differentiation through inactivation of Wnt/β-catenin signaling pathway in rat osteoblasts.

Environ Toxicol Pharmacol 2016 Mar 8;42:198-204. Epub 2015 Dec 8.

College of Veterinary Medicine, Northeast Agricultural University, NO. 59 Mucai Street, Xiangfang District, Harbin 150030, China. Electronic address:

Exposure to aluminum (Al) suppresses bone formation. Osteoblastic differentiation plays a key role in the process of bone formation. However, the effect of Al on osteoblastic differentiation is still controversial, and the mechanism remains unclear. To investigate the effect of Al on osteoblastic differentiation and whether Wnt signaling pathway was involved in it, the primary rat osteoblasts were exposed to 1/40 IC50, 1/20 IC50 and 1/10 IC50 of aluminum trichloride (AlCl3) for 24h, respectively. The activity analysis of alkaline phosphate, qRT-PCR analysis of type I collagen, alkaline phosphate, Wnt3a and Dkk-1, Western blot analysis of p-GSK3β, GSK3β and β-catenin protein and Immunofluorescence staining for β-catenin suggested that AlCl3 inhibited osteoblastic differentiation and Wnt/β-catenin pathway. Moreover, we found exogenous Wnt3a application reversed the inhibitory effect of AlCl3 on osteoblastic differentiation, accompanied by activating the Wnt/β-catenin pathway. Taken together, these findings suggest that AlCl3 inhibites osteoblastic differentiation through inactivation of Wnt/β-catenin pathway in osteoblasts.
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http://dx.doi.org/10.1016/j.etap.2015.11.023DOI Listing
March 2016

Aluminum trichloride impairs bone and downregulates Wnt/β-catenin signaling pathway in young growing rats.

Food Chem Toxicol 2015 Dec 22;86:154-62. Epub 2015 Oct 22.

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Harbin Pharmaceutical Group Bio-vaccine Limited Liability Company, Harbin 150069, China.

Aluminum (Al) can accumulate in bone and cause bone diseases. Few studies have investigated molecular mechanism of Al-induced bone diseases. Thus, in this study, rats were orally exposed to 0 (control group) and 0.4 g/L aluminum trichloride (AlCl3) (treatment group) for 30, 60, 90 or 120 days, respectively. The Al content of femora and serum, bone histological structure, bone mineral density (BMD) of the distal and proximal femoral metaphysis and Wnt/β-catenin signaling pathway (the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5) in rat femora were determined on day 30, 60, 90 or 120, respectively. The results showed that the Al contents of femora and serum were increased, the BMD of the distal and proximal femoral metaphysis were decreased, the femora histological structure were disrupted, the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5 were all decreased in the treatment group compared with the control group with time prolonged. These results indicated that AlCl3 impaired femora by inhibiting the Wnt/β-catenin signaling pathway in young growing rats.
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http://dx.doi.org/10.1016/j.fct.2015.10.005DOI Listing
December 2015

cAMP/PKA Signaling Pathway Induces Apoptosis by Inhibited NF-κB in Aluminum Chloride-Treated Lymphocytes In Vitro.

Biol Trace Elem Res 2016 Apr 18;170(2):424-31. Epub 2015 Aug 18.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.

To explore the apoptosis mechanism in lymphocytes of rats induced by aluminum chloride (AlCl3) by activating cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway, the splenic lymphocytes of rats were cultured and exposed to different concentrations of AlCl3 for 24 h. The final concentrations of AlCl3 (AlCl3 · 6H2O) in supernatant were 0 (control group, CG), 0.3 mmol/L (low-dose group, LG), 0.6 mmol/L (mid-dose group, MG), and 1.2 mmol/L (high-dose group, HG), respectively. Lymphocytes Apoptosis rate, intracellular cAMP content, PKA, survivin, B cell lymphoma/leukemia-2 (Bcl-2) and Bcl-2-associated X protein (Bax) mRNA expressions, and the mRNA and protein expressions of nuclear factor-κ-gene binding (NF-κB, p65) were detected, respectively. The results showed that apoptosis index of lymphocytes, cAMP content in intracellular and PKA mRNA expression were significantly upregulated, whereas NF-κB and survivin mRNA expressions, nuclear NF-κB (p65) protein expression, and the ratio of Bcl-2 and Bax mRNA expression were downregulated in the AlCl3-treated groups compared with those in CG. The results indicated that the activated cAMP/PKA signaling pathway induces apoptosis by inhibited NF-κB in AlCl3-treated lymphocytes in vitro.
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http://dx.doi.org/10.1007/s12011-015-0461-xDOI Listing
April 2016