Research Article Details
| Article ID: | A43107 |
| PMID: | 32553811 |
| Source: | Eur J Pharmacol |
| Title: | The effect of emodin on liver disease -- comprehensive advances in molecular mechanisms. |
| 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 by acting 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. |
| DOI: | 10.1016/j.ejphar.2020.173269 |
| Strategy ID | Therapy Strategy | Synonyms | Therapy Targets | Therapy Drugs | |
|---|---|---|---|---|---|
| S02 | Enhance lipid metabolism | triglyceride-lowering; lipid tolerance; lipid metabolism | 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) inhibitor; Decreases intestinal cholesterol absorption; FXR agonist; ACC inhibitor; FAS inhibitor; DGAT2 inhibitor; SCD-1 inhibitor | Atorvastatin; Ezetimibe; Obeticholic Acid; GS-9674; GS-0976; TVB-2640; IONIS-DGAT2rx; Aramchol; | Details |
| S03 | Anti-fibrosis | fibrosis | Angiotensin Receptor Blocker (ARB); CCR2/CCR5 antagonist; Thyroid receptor β agonist; PEGylated human FGF21 analogue; Monoclonal antibody to lysyl oxidase-like 2 (LOXL2); Galectin-3 inhibitor; FGF19 variant | Losartan; Cenicriviroc; VK-2809; MGL-3196; Pegbelfermin; Simtuzumab; GR-MD-02; NGM282 | Details |
| S04 | Anti-oxidative stress | oxidative stress | α-tocopherol: antioxidant | Vitamin E | Details |
| S05 | Anti-inflammatory | inflammatory | Bile acid; TNF-a inhibitor; Dual PPAR-α and -δ agonists; Toll-Like Receptor; (TLR)-4 antagonist; Caspase inhibitor; ASK-1 inhibitor | Ursodeoxycholic Acid; Pentoxifylline; Elafibranor; JKB-121; Emricasan; Selonsertib; | Details |
| S10 | Liver transplantation | -- | -- | -- | Details |
| S13 | Anti-apoptosis | hepatocyte apoptosis; hepatic autophagy; apoptosis | Pan-caspase inhibitor | Emricasan | Details |
| Target ID | Target Name | GENE | Action | Class | UniProtKB ID | Entry Name |
|---|
| Diseases ID | DO ID | Disease Name | Definition | Class |
|---|
| Drug ID | Drug Name | Type | DrugBank ID | Targets | Category | Latest Progress | |
|---|---|---|---|---|---|---|---|
| D579 | Emfilermin | Miscellany | -- | adipocytes | Enhance lipid metabolism | Under investigation | Details |
| D596 | Emodin | Chemical drug | -- | DNA synthesis inhibitors; Protein synthesis inhibitors; Protein tyrosine kinase inhibitors; RNA synthesis inhibitors | Anti-fibrosis | Under investigation | Details |