Ginsenoside Rg3 attenuates cisplatin‐induced kidney injury through inhibition of apoptosis and autophagy‐inhibited NLRP3. Issue 11 (23rd August 2021)

• Record Type: Journal Article
• Authors: Zhai, Jinghui; Gao, Huan; Wang, Shuo; Zhang, Sixi; Qu, Xiaoyu; Zhang, Yueming; Tao, Lina; Sun, Jingmeng; Song, Yanqing; Fu, Li
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 35:Issue 11(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-08-23
• Subjects: autophagy -- cisplatin -- ginsenoside Rg3 -- kidney injury -- nod‐like receptor protein 3; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.22896
• Languages: English
• ISSNs: 1095-6670

Abstract

Abstract: The NOD‐like receptor family pyrin domain‐containing (NLRP3) inflammasomes is centrally implicated in cisplatin (CP)‐induced kidney injury. Autophagy is critical for inhibiting production of NLRP3 protein that effectively reduces the inflammatory response. Ginsenoside Rg3 (SY), an active component extracted from ginseng, is reported to protect against CP‐induced nephrotoxicity. However, the mechanisms underlying renoprotection by SY have not been established to date. Our results indicate that SY attenuated CP‐induced apoptosis and damage in vivo and in vitro, as evidenced by increased cell viability, decreased the proportion of late apoptotic cells, elevated mitochondrial membrane potential, and ameliorated histopathological damage of the kidney. SY ameliorated CP‐induced human renal tubular (HK‐2) cells and kidney injury through upregulation of LC3II/I and beclin‐1, inhibition of p62, NLRP3, ASC, caspase‐1, and interleukin‐1β. However, blockade of autophagy by 3‐methyladenine reversed the suppression of SY on NLRP3 inflammasome activation and the protection of SY on HK‐2 cells. Our collective results support the utility of SY as a therapeutic agent that effectively protects against CP‐induced kidney injury by activating the autophagy‐mediated NLRP3 inhibition pathway.