Terminalia belerica fruit extract (TB 400 mg / kg, po for five days) and its active principle: gallic acid (GA 200 mg / kg, po for five days) were studied against carbon tetrachloride (CCl4 0.15 ml / kg, ip for 21 days) induced liver injury in rats. Toxicants increased blood sugar and serum protein (P 0.05). Induced liver necrosis increased liver-maker enzyme activity (AST, ALT, SALP and LDH), oxidative stress parameters and histopathology including necrosis, hepatocyte degeneration and inflammatory cell infiltration. CCl4 increased albumin and bilirubin. Carbon tetrachloride intoxication altered urea and creatinine. GA and LA therapy was effective, with values close to control and comparable to silymarin. At 0.15 ml/kg i.p. for 21 days, carbon tetrachloride increased hepatic triglycerides and serum cholesterol (P 0.05). Hepatic lipid peroxidation increased. CCl4 decreased reduced glutathione. CCl4 harmed succinic dehydrogenase, adenosine triphosphatase, acid and alkaline phosphatases. GA and LA reduced oxidative damage from CCl4 gallic acid and lipoic acid synergized. GA and LA acid improved liver function and oxidative stress markers. The current findings suggest that five-day GA and LA treatment could prevent liver injury in rats.
Jadon et al. (Sun,) studied this question.
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