Its ability to quench free radicals of 1,1-diphenyl-1-picrylhydrazyl, decrease the
Its ability to quench free radicals of 1,1-diphenyl-1-picrylhydrazyl, decrease the leakage of lactate dehydrogenase and ALT and prevent the formation of malondialdehyde induced by t-BHP [11]. Janbaz and Gilani reported that post-treatment with berberine (4 mg/kg) after CCl4-induced hepatotoxicity exhibited no effect in reducing hepatic damage [10]. Sun et al., however, reported that berberine protected liver injury evidenced by decreased ALT and AST activities and that berberine’s action was focused on liver fibrosis in CCl 4 -induced rats [12]. The apparent discrepancy between the two studies may be due to the dosages, animal species and animal models used. The present study found that berberine had both preventive and curative effects on CCl4-induced liver damage. Moreover, our findings suggest that dosages may be an important factor for curative effects of berberine. The dosage (4 mg/kg) used by Janbazour et al. was far below the effective dosage (80-160 mg/kg) reported in this study, which was determined according to our clinical experience [13] and was similar to the dosage reported by Sun et al. [12]. Pre-treatment of berberine significantly decreased both serum ALT and AST activities elevated by CCl4-induced hepatoxicity while serum SOD level significantly decreased (Figures 3 and 4). These results demonstrate the preventive hepatoprotective effects of berberine against liver damage induced by CCl4, further supported by the histological changes (Figure 5f).Figure 4 Effects of berberine pre-treatment on serum SOD activity in rats with CCl4 -induced acute liver damage. **P < 0.001 vs normal control; ##P <0.001 vs CCl4 control; mean (SD), n = 8.Conclusion The present study finds that berberine possesses hepatoprotective activities against CCl4-induced hepatotoxicity in a dose-dependent manner. The heptoprotective activities are both preventive and curative. These findings were further supported by the histological changes in the liver. Berberine should be a lead for developing new drugs to treat drug/chemical-induced liver toxicity.Feng et al. Chinese Medicine 2010, 5:33 http://www.cmjournal.org/content/5/1/Page 5 ofFigure 5 Photomicrography of liver sections of rats. a. liver sections of normal rats treated with olive oil vehicle only; b. liver section of the control rat treated with CCl4 only; c. liver section of the CCl4-treated rat post-treated by berberine at 160 mg/kg; d. liver section of the CCl4treated rat post-treated by berberine at 120 mg/kg; e. liver section of the CCl4-treated rat post-treated by berberine at 80 mg/kg; f. liver section of the CCl4-treated rat pre-treated by berberine at 120 mg/kg twice daily PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26162776 for two days (H E stain, original magnification ?00).Feng et al. Chinese Medicine 2010, 5:33 http://www.cmjournal.org/content/5/1/Page 6 ofTable 1 Microscopic observation on protective and preventive effects of berberine against CCl4-induced acute liver damage in rats (n = 8)Group Fatty degeneration Mean (SD) 0.6 (0.3) 5.5 (1.2)** Vacoulisation Mean (SD) 0.3 (0.2) 4.8 (0.4) ** Nuclei Mean (SD) 1.3 (0.3) 0.3 (0.2) ** Hepatocyte necrosis Mean (SD) 0.5 (0.1) 5.7 (1.9) ** Inflammatory cells infiltration Mean (SD) 0.7 (0.3) 5.5 (1.5) ** Central vein and portal triad Mean (SD) 2.2 (0.6) 0.4 (0.2) ** PF-04418948 supplier Combined score Mean (SD) 1.2 (0.3) 4.7 (0.9)##Normal CCl4 Post-treated with berberine 80 mg/kg 120 mg/kg 160 mg/kg Pre-treated with berberine 120 mg/kg3.2 (1.6) 1.7 (1.3) 1.4 (0.9)##2.5 (0.7) 1.8 (0.2) 1.2 (0.4)## ## ##1.7 (0.
