期刊
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
卷 25, 期 3, 页码 1645-1660出版社
WILEY
DOI: 10.1111/jcmm.16267
关键词
autophagy; levo-tetrahydropalmatine; liver fibrosis; PPAR gamma/NF-kappa B; TGF-beta 1/Smad
资金
- Yangfan Project of Shanghai Science and Technology Commission [20YF1443300]
- Natural Science Foundation of Shanghai [19ZR1447700]
- Health System Innovation Project of Shanghai Putuo Science and Technology Commission [PTKWWS201801, PTKWWS201903]
- WBN Hepatology Research Fund of China Hepatitis Prevention and Treatment Foundation [CFHPC2019031]
- National Natural Science Foundation of China [81670472]
- Foundation of Minhang Hospital [2018MHJC08]
Levo-tetrahydropalmatine alleviates liver fibrosis by inhibiting extracellular matrix formation and hepatic stellate cells' autophagy, as well as modulating key signaling pathways, ultimately attenuating the progression of liver fibrosis.
Liver fibrosis is a necessary stage in the development of chronic liver diseases to liver cirrhosis. This study aims to investigate the anti-fibrotic effects of levo-tetrahydropalmatine (L-THP) on hepatic fibrosis in mice and cell models and its underlying mechanisms. Two mouse hepatic fibrosis models were generated in male C57 mice by intraperitoneal injection of carbon tetrachloride (CCl4) for 2 months and bile duct ligation (BDL) for 14 days. Levo-tetrahydropalmatine was administered orally at doses of 20 and 40 mg/kg. An activated LX2 cell model induced by TGF-beta 1 was also generated. The results showed that levo-tetrahydropalmatine alleviated liver fibrosis by inhibiting the formation of extracellular matrix (ECM) and regulating the balance between TIMP1 and MMP2 in the two mice liver fibrosis models and cell model. Levo-tetrahydropalmatine inhibited activation and autophagy of hepatic stellate cells (HSCs) by modulating PPAR gamma/NF-kappa B and TGF-beta 1/Smad pathway in vivo and in vitro. In conclusion, levo-tetrahydropalmatine attenuated liver fibrosis by inhibiting ECM deposition and HSCs autophagy via modulation of PPAR gamma/NF-kappa B and TGF-beta 1/Smad pathway.
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