Abstract Title:

Effects of gastrodin against carbon tetrachloride induced kidney inflammation and fibrosis in mice associated with the AMPK/Nrf2/HMGB1 pathway.

Abstract Source:

Food Funct. 2020 May 1 ;11(5):4615-4624. Epub 2020 May 13. PMID: 32400831

Abstract Author(s):

Jie-Qiong Ma, Yun-Zhi Sun, Qing-Lei Ming, Zhi-Kai Tian, Yu-Jia Zhang, Chan-Min Liu

Article Affiliation:

Jie-Qiong Ma


Gastrodin (GAS), the main phenolic glycoside extracted from Gastrodia elata Blume, exhibits potential renoprotective properties. Here, we examined the protective effects of GAS on carbon tetrachloride (CCl)-induced kidney inflammation and fibrosis in mice, and explored its underlying mechanisms. Our research findings revealed that GAS improved CCl-induced renal damage in mice. GAS inhibited kidney fibrosis and the deposition of collagen andα-smooth muscle actin (α-SMA). GAS suppressed CCl-induced inflammation in kidney tissue, as indicated by the decreased levels of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). The renoprotective effects of GAS were associated with inhibiting oxidative stress by regulating nuclear factor-erythroid 2-related factor 2 (Nrf2)-mediated antioxidant signaling and increasing adenosine 5'-monophosphate activated protein kinase (AMPK) activation. Furthermore, GAS supplementation inactivated the receptor for advanced glycation end products (RAGE) and the high-mobility group box-1 (HMGB1) pathway. GAS inhibited the activation of Toll-like receptors (TLRs), nuclear factor-kappa B (NF-κB) and transforming growth factor (TGF)-β. Collectively, this study clarified that GAS attenuates CCl-induced kidney inflammation and fibrosis via the AMPK/Nrf2/HMGB1 pathway.

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