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Yu, Yani, Dong, Hui, Sun, Jingyi, Li, Baoshuang, Chen, Yueqi, Feng, Moxuan, Yang, Xiaoqian, Jiang, Wei. (1400). Hepatitis B virus X mediates podocyte pyroptosis by regulating the ROS/NLRP3 signaling pathway in hepatitis B virus-associated glomerulonephritis. , 25(1), 103-109. doi: 10.22038/ijbms.2022.61105.13520
Yani Yu; Hui Dong; Jingyi Sun; Baoshuang Li; Yueqi Chen; Moxuan Feng; Xiaoqian Yang; Wei Jiang. "Hepatitis B virus X mediates podocyte pyroptosis by regulating the ROS/NLRP3 signaling pathway in hepatitis B virus-associated glomerulonephritis". , 25, 1, 1400, 103-109. doi: 10.22038/ijbms.2022.61105.13520
Yu, Yani, Dong, Hui, Sun, Jingyi, Li, Baoshuang, Chen, Yueqi, Feng, Moxuan, Yang, Xiaoqian, Jiang, Wei. (1400). 'Hepatitis B virus X mediates podocyte pyroptosis by regulating the ROS/NLRP3 signaling pathway in hepatitis B virus-associated glomerulonephritis', , 25(1), pp. 103-109. doi: 10.22038/ijbms.2022.61105.13520
Yu, Yani, Dong, Hui, Sun, Jingyi, Li, Baoshuang, Chen, Yueqi, Feng, Moxuan, Yang, Xiaoqian, Jiang, Wei. Hepatitis B virus X mediates podocyte pyroptosis by regulating the ROS/NLRP3 signaling pathway in hepatitis B virus-associated glomerulonephritis. , 1400; 25(1): 103-109. doi: 10.22038/ijbms.2022.61105.13520

Hepatitis B virus X mediates podocyte pyroptosis by regulating the ROS/NLRP3 signaling pathway in hepatitis B virus-associated glomerulonephritis

Iranian Journal of Basic Medical Sciences
مقاله 14، دوره 25، شماره 1، فروردین 2022، صفحه 103-109    اصل مقاله (596.67 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2022.61105.13520
نویسندگان
Yani Yu1؛ Hui Dong2؛ Jingyi Sun1؛ Baoshuang Li1؛ Yueqi Chen1؛ Moxuan Feng1؛ Xiaoqian Yang1؛ Wei Jiang* 1
1Department of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong, China
2Health Management Center, The Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong, China
چکیده
Objective(s): This study was designed to investigate whether HBx-induced podocyte injury is related to the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome and the specific mechanism of the oxidative stress pathway in hepatitis B virus-associated glomerulonephritis (HBV-GN).
Materials and Methods: The HBx gene was overexpressed in renal podocytes to mimic HBV-GN. Podocyte morphology was observed under a scanning electron microscope. Reactive oxygen species (ROS) generation was detected by dichlorodihydrofluorescein diacetate (DCFH-DA) assay. The podocytes in each group were treated with Hoechst 33342 and subjected to immunofluorescence staining. Caspase-1 activity and LDH levels were assessed with a Caspase-1 Activity Assay Kit and an LDH ELISA Kit, respectively. The expression of all pyroptosis-related proteins was examined by Western blot analysis.
Results: Pyroptosis-related proteins, including NLRP3, apoptosis-associated speck-like protein containing card (ASC), caspase-1, IL-1β, and IL-18 (P<0.05), were up-regulated upon HBx overexpression, and caspase-1 enzyme activity and LDH and Desmin expression were also enhanced (P<0.05). NLRP3 knockdown attenuated the increased expression of pyroptosis-related proteins upon HBx overexpression (P<0.05), which was also achieved by the addition of an ROS inhibitor (P<0.05).
Conclusion: HBx regulates podocyte pyroptosis in HBV-GN by targeting the NLRP3 inflammasome, and mitochondrial oxidative stress plays an important role in this process.
کلیدواژه‌ها
Glomerulonephritis؛ HBx؛ NLRP3؛ Pyroptosis؛ ROS
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