Methanolic extract of Woodfordia fruticosa Kurz flowers ameliorates carbon tetrachloride-induced chronic hepatic fibrosis in rats.

Hepatic fibrosis, characterized by extracellular matrix accumulation, is the common cause of chronic liver failure and is a leading cause of morbidity and mortality worldwide. The aim of the present study was to evaluate the effect of dried flowers of Woodfordia fruticosa on carbon tetrachloride (CCl4)-induced hepatic fibrosis in rat model. Hepatic fibrosis was induced in male Wistar rats by CCl4 administration (150 µl/100 g rat weight, oral) twice a week for 10 weeks. In preventive model, administration of daily doses of methanolic extract of W. fruticosa (MEWF) at two different doses (100 mg/kg, body weight (b.w.) and 200 mg/kg, b.w.) was started 1 week before the onset of CCl4 administration and continued for 10 weeks. In curative model, MEWF at 100 and 200 mg/kg were given for last 2 weeks after the establishment of fibrosis. MEWF at a dose of 200 mg/kg was able to exert a more pronounced effect as evidenced histologically by significant reduction in fibrotic septa formation in liver tissue, immunohistochemically by abridged expression of collagen III, and also biochemically by serum and tissue antioxidant status, lipid peroxidation, and hydroxyproline level. Liquid chromatography-mass spectrometry analysis revealed the presence of confertin, quercetin methyl ether, ellagic acid, and stigmasterol in MEWF, which could be responsible for its antifibrotic activity. These results indicate the effective protection exerted by MEWF against CCl4-induced hepatic fibrosis in a dose-dependent manner.

Dose-response effects of Elephantopus scaber methanolic extract on N-nitrosodiethylamine-induced hepatotoxicity in rats.

AIM: A decoction of Elephantopus scaber (Asteraceae) root is used to treat liver disorders in Indian and Chinese traditional medicine. The study was designed to examine the dose response effects of E. scaber methanolic extract on rats exposed to N-nitrosodiethylamine (NDEA) induced hepatotoxicity (0.02% NDEA in water five days per week, per oral) in preventive and curative models. METHODS: In preventive groups, NDEA was administered for six weeks. Daily doses of E. scaber methanolic extract (200 and 100 mg·kg-1) started one week before the onset of NDEA intoxication and continued for six weeks. In curative animals, NDEA was administered for six weeks followed by treatment with the methanolic n-hexane extract of E. scaber (200 and 100 mg·kg-1) for ten days. RESULTS: E. scaber extract treatment significantly (P ≤ 0.05) reduced the levels of AST, ALT, and MDA in both experimental groups. The extract also enhanced the antioxidant enzyme and protein levels in rats intoxicated with NDEA. Treatment with the extract dose dependently protected the liver from NDEA-induced hepatotoxicity with normal hepatocytes and uniform sinusoids, but in some areas showed degenerating hepatic cells in both treatment groups. CONCLUSION: E. scaber methanolic extract dose dependently prevented and reversed the hepatotoxicity induced by NDEA in both experimental models.