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目的探讨新疆鼠尾草总酚酸对糖尿病大鼠肾脏蛋白激酶C(PKC)活性的影响。方法将60只雄性SD大鼠随机分为正常组(A)10只和造模组50只,采用高脂饲料加链脲佐菌素(STZ)腹腔注射建立糖尿病大鼠模型,造模成功后随机分为5组:糖尿病模型组(B)、盐酸二甲双胍组(C)及新疆鼠尾草总酚酸低(D)、中(E)、高(F)剂量组,每组10只。干预8 w,检测大鼠肾脏指数、血糖、肌酐清除率(Ccr)、尿白蛋白排泄率(UAER)、肾脏PKC活性。结果与正常组比较,模型组大鼠肾脏指数、血糖、Ccr、UAER和肾脏细胞膜PKC活性均明显升高,差异有统计学意义(P<0.05);与模型组比较,盐酸二甲双胍组和新疆鼠尾草总酚酸高剂量组大鼠肾脏指数、血糖、Ccr、UAER和肾脏细胞PKC活性均明显下降,差异有统计学意义(P<0.05);新疆鼠尾草总酚酸低剂量组大鼠的血糖明显下降,差异有统计学意义(P<0.05),其余指标无明显下降,差异无统计学意义;新疆鼠尾草总酚酸中剂量组大鼠的血糖、UAER、肾脏细胞膜PKC明显下降,差异有统计学意义(P<0.05),其余指标无明显下降,差异无统计学意义。结论新疆鼠尾草总酚酸能保护糖尿病肾病(DN)大鼠肾脏,其作用机制与抑制其肾脏PKC的激活有关。
Objective To investigate the effect of total salvianolic acid on protein kinase C (PKC) activity in diabetic rats. Methods Sixty male Sprague-Dawley rats were randomly divided into normal group (A) 10 and model group 50 rats. Diabetic rats were induced by intraperitoneal injection of high-fat diet plus streptozotocin (STZ) The rats were randomly divided into 5 groups: diabetic model group (B), metformin hydrochloride group (C) and Salvia przewalskii (D), medium (E) and high (F) After intervention for 8 weeks, the renal index, blood glucose, creatinine clearance rate (Ccr), urinary albumin excretion rate (UAER) and renal PKC activity were detected. Results Compared with the normal group, the renal index, blood glucose, Ccr, UAER and PKC activity in the kidney of model group were significantly increased (P <0.05). Compared with the model group, the metformin hydrochloride group The contents of kidney index, blood glucose, Ccr, UAER and the PKC activity of renal cells were significantly decreased in high dose of total salvianolic acid group (P <0.05) (P <0.05), but the other indexes did not decrease significantly, the difference was not statistically significant; blood glucose, UAER, PKC of kidney cell membrane of rats were significantly decreased , The difference was statistically significant (P <0.05), the other indicators no significant decline, the difference was not statistically significant. Conclusion Salicylic acid total phenolic acid can protect the kidneys of diabetic nephropathy (DN) rats, and its mechanism may be related to inhibiting the activation of PKC in the kidney.