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The chalcone butein from Rhus verniciflua shows antifibrogenic activity
Sung Hee Lee1, Ji-Xing Nan, Yu Zhe Zhao
1College of Pharmacy, Medicinal Resources Research Center, Wonkwang University, Iksan, Chonbuk, Republic of Korea.
Planta Medica
|January 22, 2004
Summary
Butein, a compound from Rhus verniciflua, effectively reduces liver fibrosis in rats by inhibiting collagen and lipid peroxidation. It also down-regulates key fibrotic gene expressions, showing potential as an antifibrogenic agent.
Area of Science:
- Pharmacology
- Hepatology
- Natural Products Chemistry
Background:
- Liver fibrosis is a significant health concern.
- Carbon tetrachloride (CCl4) is a common inducer of experimental liver fibrosis.
- Rhus verniciflua Stokes (Anacardiaceae) contains butein, a potential therapeutic compound.
Purpose of the Study:
- To investigate the antifibrogenic effects of butein on CCl4-induced liver fibrosis in rats.
- To elucidate the underlying antifibrogenic mechanisms of butein.
Main Methods:
- Rats were induced with liver fibrosis using CCl4.
- Butein was administered at doses of 10 mg/kg/day and 25 mg/kg/day.
- Hydroxyproline, malondialdehyde, alpha1(I) collagen mRNA, and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA levels were measured.
Main Results:
- Butein significantly reduced hydroxyproline and malondialdehyde levels.
- A dose-dependent reduction in alpha1(I) collagen and TIMP-1 mRNA expression was observed.
- Butein demonstrated significant antifibrotic activity.
Conclusions:
- Butein exhibits potential as an antifibrogenic agent.
- Its mechanism involves inhibiting collagen accumulation and lipid peroxidation.
- Down-regulation of alpha1(I) collagen and TIMP-1 mRNA expression contributes to its effects.