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Suppression of SIRT1/FXR signaling pathway contributes to oleanolic acid-induced liver injury
In conclusion, our study reveals that SIRT1/FXR pathway is crucial in OA-induced hepatotoxicity. Activation of SIRT1/HNF1α/FXR axis may represent a novel therapeutic target for ameliorating OA and other herb-induced hepatotoxicity.PMID:37028458 | DOI:10.1016/j.taap.2023.116509
Source: Toxicology and Applied Pharmacology - April 7, 2023 Category: Toxicology Authors: Songjie Liao Xiaolong Fu Jianxiang Huang Yi Wang Yuanfu Lu Shaoyu Zhou Source Type: research

Vitexin attenuates autoimmune hepatitis in mouse induced by syngeneic liver cytosolic proteins via activation of AMPK/AKT/GSK-3 β/Nrf2 pathway
In conclusion, vitexin ameliorated hepatic injury in EAH mice through activation of the AMPK/AKT/GSK-3β pathway and upregulation of the Nrf2 gene.PMID:34953801 | DOI:10.1016/j.ejphar.2021.174720
Source: European Journal of Pharmacology - December 26, 2021 Category: Drugs & Pharmacology Authors: Lei Zhang Dazhi Chen Yulu Tu Tiantian Sang Tongtong Pan Hongwei Lin Chao Cai Xiaozhi Jin Faling Wu Lanman Xu Yongping Chen Source Type: research

Ephedrine-induced mitophagy via oxidative stress in human hepatic stellate cells.
In this study, we investigated hepatotoxicity and key regulation of mitophagy in ephedrine-treated LX-2 cells. Ephedrine triggered mitochondrial oxidative stress and depolarization. Mitochondrial swelling and autolysosome were observed in ephedrine-treated cells. Ephedrine also inhibited mitochondrial biogenesis, and the mitochondrial copy number was decreased. Parkin siRNA recovered the ephedrine-induced mitochondrial damage. Excessive mitophagy lead to cell death through imbalance of autophagic flux. Moreover, antioxidants and reducing Parkin level could serve as therapeutic targets for ephedrine-induced hepatotoxicity. ...
Source: Journal of Toxicological Sciences - July 21, 2017 Category: Toxicology Tags: J Toxicol Sci Source Type: research

Acetylshikonin induces apoptosis of hepatitis B virus X protein-expressing human hepatocellular carcinoma cells via endoplasmic reticulum stress.
Abstract Since it has been known that shikonin derived from a medicinal plant possesses anti-cancer activity, we wonder whether acetylshikonin (ASK), a derivate of shikonin, could be used to treat hepatocellular carcinoma cells expressing hepatitis B virus X protein (HBX), an oncoprotein from hepatitis B virus. When ASK was added to Hep3B cells stably expressing HBX, it induced apoptosis in a dose-dependent manner. ASK induced upregulation and export of Nur77 to the cytoplasm and activation of JNK. Likewise, suppression of Nur77 and JNK inactivation protected the cells from ASK-induced apoptosis, indicating that N...
Source: European Journal of Pharmacology - April 24, 2014 Category: Drugs & Pharmacology Authors: Moon J, Koh SS, Malilas W, Cho IR, Kaewpiboon C, Kaowinn S, Lee K, Jhun BH, Choi YW, Chung YH Tags: Eur J Pharmacol Source Type: research