Effects of Buyang Huanwu Decoction on renal oxidative stress and NF-κB pathway in diabetic nephropathy rats / 国际中医中药杂志

ABSTRACT

Objective:To observe the effect of Buyang Huanwu Decoction on renal oxidative stress and NF-κB pathway in diabetic nephropathy rats.Methods:Sixty SD rats were randomly divided into normal group, model group, low, medium, and high dose of Buyang Huanwu Decoction groups and metformin group, with 10 rats in each group. The normal group was given ordinary diet every day, and the other groups were given high-fat and high-sugar diet for 6 weeks, then intraperitoneally injected 35 mg/kg STZ to establish diabetic nephropathy model. After successful modeling, the rats were orally injected with 7.42, 14.84 and 29.68 g/kg of low-dose, medium-dose and high-dose Buyang Huanwu Decoction and metformin group was orally given metformin solution 0.2 g/kg. After 6 weeks of feeding, the body weight, 24h urinary protein, serum creatinine and urea nitrogen were detected. The levels of GSH-Px, SOD, CAT and MDA in rats' kidney of each group were detected. The protein expression levels of NF-κBp65, p-NF-κBp65, TNF-α and IL-6 in rats' kidney in each group were detected by Western Blot.Results:Compared with model group, the body weight of the low, medium and high dose of Buyang Huanwu Decoction groups were increased ( P<0.01), the content of 24 h urinary protein, serum creatinine and urea nitrogen were decreased ( P<0.05 or P<0.01),the content of GSH-Px , SOD, CAT were significantly increased ( P<0.05 or P<0.01), the content of MDA was significantly decreased ( P<0.05 or P<0.01), the expression of NF-κB p65 (0.53±0.07, 0.46±0.09, 0.42±0.10 vs. 0.67±0.13), p-NF-κB p65 (0.51±0.12, 0.43±0.06, 0.34±0.17 vs. 0.59±0.07), TNF-α (1.21±0.08, 1.17±0.04, 1.05±0.22 vs. 1.43±0.21), IL-6 (0.92±0.04, 0.89±0.25, 0.73±0.09 vs. 1.06±0.08) were significantly decreased ( P<0.05 or P<0.01). Conclusion:Buyang Huanwu Decoction can improve oxidative stress state and inflammatory damage in renal tissue. The mechanism may be related to the inhibition of NF-κB signaling pathway.