Diabetic nephropathy (DN) is the leading cause of chronic renal disease. Accumulating evidence suggested that oxidative stress and inflammatory processes are involved in the development of DN. In the present study, the DN model was established by injecting mice with STZ (180 mg*kg-1) intraperitoneally, and treated with EA (50, 100 and 150 mg*kg-1) and IRB (positive control) once daily by intragastric gavage. At the same time, rat kidney NRK-52E cells were cultured and incubated with EA and TAK-242 (inhibitor of TLR4) respectively before stimulating with LPS. The mental conditions, body weight, blood glucose, serum albumin (Alb), serum TNF-α, renal function, anti-oxidative enzymes, and protein expression of TLR4, IRAK4, TRAF6, IKKβ, NF-κb P65, HMGB1 in renal tissue were determined. Meanwhile, the proteins expression of TLR4, IRAK1 and NF-κBp65 in cells were further analyzed. The results showed that EA could improve the daily state and body weight; decrease the blood glucose, levels of TNF-α and serum creatinine; elevate the activities of antioxidant enzymes; ameliorate the renal pathology; inhibit the up regulation of expression of proteins TLR4, IRAK4, TRAF6, IKK-β, NF-κBp65 and HMGB1 in DN mice. These results suggested that EA ameliorated STZinduced oxidative renal injury by the inhibition of HMGB1-TLR4-NF-кB pathway.

糖尿病肾病（DN）是慢性肾脏疾病的主要原因。越来越多的证据表明，氧化应激和炎症过程与DN的发展有关。在本研究中，通过向小鼠腹膜内注射STZ（180 mg * kg-1）建立DN模型，并每天一次通过EA（50、100和150 mg * kg-1）和IRB（阳性对照）进行治疗，胃内灌胃。同时，在用LPS刺激之前，将大鼠肾NRK-52E细胞培养并分别与EA和TAK-242（TLR4的抑制剂）一起温育。肾脏组织中的精神状况，体重，血糖，血清白蛋白（Alb），血清TNF-α，肾功能，抗氧化酶和TLR4，IRAK4，TRAF6，IKKβ，NF-κbP65，HMGB1的蛋白表达被确定。同时，TLR4的蛋白质表达 进一步分析了细胞中的IRAK1和NF-κBp65。结果表明，电针可以改善日常状态和体重。降低血糖，TNF-α和血清肌酐水平；增强抗氧化酶的活性；改善肾脏病理；抑制DN小鼠中TLR4，IRAK4，TRAF6，IKK-β，NF-κBp65和HMGB1蛋白的表达上调。这些结果表明，EA通过抑制HMGB1-TLR4-NF-кB途径改善了STZ诱导的氧化性肾损伤。