Berberine conveyed antioxidative effect via down- and up-regulation of GPx and CuZn-SOD expression, respectively. Therefore, use of berberine as a hypoglycemic compound for alternative treatment of DM could bring extra-beneficent consequence according to its antioxidative stress.

Context: Diabetes mellitus (DM) type 2 is a chronic disease characterized by hyperglycemia and insulin resistance. Oxidative stress participates in development and progression of DM, in which changes of superoxide dismutase (SOD) and catalase (CAT) were noted in DM mice. Berberine has been widely used as an alternative medicine and proved to be effective for the treatment of DM and dyslipidemia. Objective: Impacts of berberine on transcriptional regulation of SOD and CAT and their enzyme activities, including the level of malondialdehyde (MDA) formation, were examined in the DM type 2-induced mice to clarify its antioxidation potential, compared with a common hypoglycemic drug, glibenclamide. Materials and methods: Noninsulin-dependent diabetes was induced in mice by a single intraperitoneal streptozotocin-nicotinamide injection. Diabetic mice were treated daily with glibenclamide (10 mg/kg/d) and/or berberine (100 mg/kg/d) for 2 weeks. The fasting blood glucose and the MDA levels in the mouse liver, brain and kidneys were monitored using Glucometer Õ (Accu-Check Õ Advantage II Performa kits, Roche Diagnostics, Germany) and thiobarbituric acid substance assay, respectively. The expression of SOD and CAT mRNA were determined in the mouse liver and the activities of SOD and CAT enzymes were determined in mouse liver, brain and kidneys, respectively. Results: Berberine exhibited similar hypoglycemic potential as glibenclamide to lower area under the curve of the fasting blood glucose. In DM type 2 mice, berberine increased the hepatic CuZn-SOD mRNA expression and the kidney SOD and CAT activities to normal levels. Moreover, DM-induced lipid peroxidation by increasing of MDA levels in both the liver and brain and lipid peroxidation status was restored by berberine. Conclusion: Berberine possessed hypoglycemic properties and strong potential to improve the oxidant-antioxidant balance, though the combination treatment of berberine and glibenclamide did not show additional benefit over the treatment with berberine alone.

The aims of the present study were to determine cytochrome P450 enzyme activity in six strains of experimental rodents (n = 5/sex/species): ICR, C57BL/6 and DBA/2 mice; Sprague Dawley and Wistar rats; and Dunkin Hartley guinea pigs. After animals were treated with the typical inducers β-naphthoflavone (BNF), dexamethasone (DEX) and phenobarbital (PB), the levels of O-dealkylation of ethoxyresorufin (EROD), methoxyresorufin (MROD), pentoxyresorufin (PROD) and benzyloxyresorufin (BROD) activity were determined using responsive catalytic reactions to study CYP1A1, CYP1A2 and CYP2B, respectively. A maximal induction of EROD and MROD was found in BNF-treated animals from all strains (2.4- to 15.1-fold) except DBA/2 (0.9- to 1.8-fold). C57BL/6 mice had the strongest BNF-induced EROD (15.1-fold) and MROD (8.3-fold) activities. No differences in BNF-induced EROD and MROD activities were observed between males and females. However, the EROD activity of Wistar rats and the MROD activity of Sprague Dawley rats were higher in males than females. DEX induced PROD activity only in mice (1.3- to 7.1-fold), but not in rats and guinea pigs (0.2- to 1.1-fold). However, induction of BROD activity was found in DEX-treated mice and rats (1.5 to 12.5-fold), but not in guinea pigs (0.3 to 0.4-fold). PB caused a significant elevation of PROD (1.7- to 10.4-fold) and BROD (31- to 13.2-fold) activities in all the animals. PB-induced BROD activity was higher in females than males in Sprague Dawley rats. These observations strongly suggest that the choice of experimental animal strain, species and inducer is of critical importance for studies of drug metabolism and interaction.

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