The role of PSMB5 in sodium arsenite–induced oxidative stress in L-02 cells
Ying Lv,Hu Qian,Mingyang Shi,Wen Wang,Yuancui Zheng,Zhong Yang,Liuyu Peng,Dingnian Bi,Aihua Zhang,Hu Yong +9 more
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TLDR
Overall, NaAsO 2 exposure could induce oxidative stress liver injury and low expression of PSMB5 in L-02 cells, andPSMB5 might play an important role in the regulation of oxidative stress by regulating the expression of SOD1 and Gpx1.Abstract:
Endemic arsenism is widely distributed in the world, which can damage multiple organs, especially in skin and liver. The etiology is clear, but the mechanisms involved remain unknown. Ubiquitin-proteasome pathway (UPP) is the main pathway regulating protein degradation of which proteasome subunit beta type-5(PSMB5) plays a dominant role. This paper aims to study the role and mechanism of PSMB5 in sodium arsenite (NaAsO2)-induced oxidative stress liver injury in L-02 cells. Firstly, L-02 cells were exposed to different concentrations of NaAsO2 to establish a liver injury model of oxidative stress, and then mechanisms of oxidative stress were studied with carbobenzoxyl-leucyl-leucl-leucll-line (MG132) and knockdown PSMB5 (PSMB5-siRNA). The oxidative stress indicators, levels of 20S proteasome, the transcription and protein expression levels of PSMB5, Cu-Zn superoxide dismutase (SOD1), and glutathione peroxidase 1 (GPx1) were detected. The results demonstrated that NaAsO2 could induce oxidative stress-induced liver injury and the activity of 20S proteasome and the protein expression of PSMB5, SOD1, and GPx1 decreased. After MG132 or PSMB5-siRNA pretreatment, the gene expression of PSMB decreased. After MG132 or PSMB5-siRNA pretreatment, and then L-02 cells were treated with NaAsO2, the gene expression of PSMB remarkably decreased; however, the protein expression of SOD1 and GPx1 increased. Overall, NaAsO2 exposure could induce oxidative stress liver injury and low expression of PSMB5 in L-02 cells, and PSMB5 might play an important role in the regulation of oxidative stress by regulating the expression of SOD1 and Gpx1.read more
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LC/MS/MS-Based Liver Metabolomics to Identify Chronic Liver Injury Biomarkers Following Exposure to Arsenic in Rats
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Protective Effect of Dictyophora Polysaccharides on Sodium Arsenite-Induced Hepatotoxicity: A Proteomics Study
Ting Hu,Liming Shen,Qun Huang,Changyan Wu,Huajie Zhang,Qibing Zeng,Guoze Wang,Shaofeng Wei,Shuling Zhang,Jun Zhang,Naseer Ullah Khan,Xiangchun Shen,Peng Luo +12 more
TL;DR: In this paper, the mechanism of sodium arsenite (NaAsO2)-induced apoptosis of human hepatic cells, and how Dictyophora polysaccharide (DIP) protects L-02 cells from arsenic induced apoptosis was investigated.
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Mechanism underlying the targeted regulation of the SOD1 3'UTR by the AUF1/Dicer1/miR-155/SOD1 pathway in sodium arsenite-induced liver injury.
Dingnian Bi,Mingyang Shi,Dan Zheng,Qian Hu,Hongling Wang,Liuyu Peng,Didong Lou,Lihua Zhang,Yong Hu +8 more
TL;DR: In this paper , the authors established a model of arsenic-induced chronic liver injury by providing rats with drinking water containing different concentrations of sodium arsenite (NaAsO2) and found that NaAsO 2 exposure decreased the mRNA and protein levels of AUF1 and the protein level of SOD1 and elevated Dicer1 and miR-155.
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PSMB5 overexpression is correlated with tumor proliferation and poor prognosis in hepatocellular carcinoma
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PSMB5 Alleviates Ulcerative Colitis by Inhibiting ROS-Dependent NLRP3 Inflammasome-Mediated Pyroptosis
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