Cytotoxicity and hepatoprotective attributes of methanolic extract of Rumex vesicarius L.

Abstract

BackgroundTo evaluate the hepatoprotective potential and invitro cytotoxicity studies of whole plant methanol extract of Rumex vesicarius L. Methanol extract at a dose of 100 mg/kg bw and 200 mg/kg bw were assessed for its hepatoprotective potential against CCl4-induced hepatotoxicity by monitoring activity levels of SGOT (Serum glutamic oxaloacetic transaminase), SGPT (Serum glutamic pyruvic transaminase), ALP (Alkaline phosphatase), TP (Total protein), TB (Total bilirubin) and SOD (Superoxide dismutase), CAT (Catalase), MDA (Malondialdehyde). The cytotoxicity of the same extract on HepG2 cell lines were also assessed using MTT assay method at the concentration of 62.5, 125, 250, 500 μg/ml.ResultsPretreatment of animals with whole plant methanol extracts of Rumex vesicarius L. significantly reduced the liver damage and the symptoms of liver injury by restoration of architecture of liver. The biochemical parameters in serum also improved in treated groups compared to the control and standard (silymarin) groups. Histopathological investigation further corroborated these biochemical observations. The cytotoxicity results indicated that the plant extract which were inhibitory to the proliferation of HepG2 cell line with IC50 value of 563.33 ± 0.8 μg/ml were not cytotoxic and appears to be safe.ConclusionsRumex vesicarius L. whole plant methanol extract exhibit hepatoprotective activity. However the cytotoxicity in HepG2 is inexplicable and warrants further study.

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Rheum palmatum root extract inhibits hepatocellular carcinoma in rats treated with diethylnitrosamine

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Antipyretic and hepatoprotective potential of Tinospora crispa and investigation of possible lead compounds through in silico approaches

“…Increased levels of SGPT, SGOT, and ALP in CCl 4 -induced animals also reflect cellular damage and diminution of cell membrane function(Zeashan et al, 2008).Lipid peroxidation is an autocatalytic process and may lead to cell death. During the lipid peroxidation process, several end products are formed, including malondialdehyde (MDA), formed during oxidative degeneration as a product of oxygen free radicals and accepted as an indicator of lipid peroxidation(Tukappa, Londonkar, Nayaka, & Kumar, 2015). MDA levels are increased by the induction of CCl 4 , which increases the rate of lipid peroxidation, thus promoting hepatic tissue damage(Huang et al, 2010).Antioxidants usually prevent the lipid peroxidation reaction in normal circumstances.…”