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Abstract Title:

The effect of emodin on liver disease -- comprehensive advances in molecular mechanisms.

Abstract Source:

Eur J Pharmacol. 2020 Sep 5 ;882:173269. Epub 2020 Jun 14. PMID: 32553811

Abstract Author(s):

Naihua Hu, Jie Liu, Xinyan Xue, Yunxia Li

Article Affiliation:

Naihua Hu

Abstract:

Liver injury could be caused by a variety of causes, including alcohol, drug poisoning, autoimmune overreaction, etc. In the period of liver injury, hepatic stellate cells (HSCs) will be activated and produce excessive extracellular matrix (ECM). If injury cannot be suppressed, liver injury will develop into fibrosis, even cirrhosis and liver cancer. It is reported that some monomer components extracted from traditional Chinese medicine have better effects on protecting liver. Emodin, an anthraquinone compound extracted from the traditional Chinese medicine RHEI RADIX ET RHIZOMA, has anti-inflammatory, antioxidant, liver protection and anti-cancer effects, and can prevent liver injury induced by a variety of factors. By searching literatures related to the liver protection of emodin in PUBMED, SINOMED, EBM and CNKI databases, it was found that emodin could inhibit the production and promote the secretion of bile acids, and have a protective effect on intrahepatic cholestasis. Also, emodin reduce collagen synthesis and anti-hepatic fibrosis by inhibiting oxidative stress, TGF-β/Smad pathway and HSCs proliferation, and promoting apoptosis of HSCs. Emodin can also regulate lipid metabolism and regulate the synthesis and oxidation of lipids and cholesterol to protect the nonalcoholic fatty liver. Besides, emodin can induce the apoptosis of hepatocellular carcinoma cells byacting on the death receptor pathway and mitochondrial apoptosis pathway, thus inhibiting the development of hepatocellular carcinoma. Moreover, emodin can modulate immunity and improve immune rejection in liver transplantation animals. In conclusion, emodin has a good effect on liver protection, but further experimental data are needed to verify it.

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