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Published:
Jul 9, 2021Keywords:
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Main Article Content
Hepatoprotective and antioxidant properties of the methanol leaf extract of <i>Diaphananthe bidens</i> in acetaminophen-induced hepatotoxicity in rats
Abstract
Purpose: To investigate the hepatoprotective and antioxidant properties of the methanol extract of Diaphananthe bidens leaf using acetaminophen-induced hepatotoxicity rat model.
Methods: Thirty albino Wistar rats, randomly assigned into 6 groups (A - F, n = 5), were used for the study. Groups A and B received distilled water (10 ml/kg), group C received silymarin (0.10 g/kg) while groups D - F received D. bidens extract 0.15, 0.30 and 0.60 g/kg, respectively, for 7 days. On day 8, groups B - F rats received acetaminophen (2 g/kg) orally. About 48 h later, pentobarbitone sodium (0.035 g/kg) was injected intraperitoneally for sleeping time studies. The time of sleep, time of awake and the duration of sleep were recorded. On awakening, blood samples were collected for evaluation of serum biochemical parameters and antioxidant profile. Thereafter, the rats were humanely euthanized and the liver excised for histopathological evaluation. In vitro antioxidant activity of the extract was evaluated using ferric reducing antioxidant power and 2,2-diphenyl-1-picrylhydrazine (DPPH) scavenging assay.
Results: Treatment of the rats with D. bidens decreased (p < 0.05) malondialdehyde values and activities of ALT, AST and ALP, but increased glutathione levels and catalase activities when compared to negative control group. The extract significantly (p < 0.05) decreased sodium pentobarbitone-induced sleeping time relative to the negative control group and produced concentration-dependent increase in antioxidant activities in vitro. The extract protected the hepatocyte against acetaminophen-induced damage.
Conclusion: D. bidens extract elicits antioxidant activities in vitro and in vivo and thus, protects rat liver against acetaminophen-induced damage. Therefore, the extract can potentially be developed as a hepatoprotective agent for the clinical management of liver damage.
