灯盏花素对糖尿病大鼠肾脏间质小动脉影响的实验研究

目的探讨灯盏花素对糖尿病大鼠肾小动脉的影响。方法选健康雄性昆明种SD大鼠70只,随机分为正常对照组（C）20只、糖尿病组（A）和糖尿病灯盏花治疗组（B）各25只。链脲菌素（streptozotocin,STZ）诱导建立糖尿病肾病大鼠模型,B组灯盏花素20mg·kg-1·d-1腹腔内注射,A组和C组等量生理盐水腹腔内注射,3组给药后2W和6W宰杀,收集血检测TGF-β1,肌酐和尿素氮水平,肾组织标本检测NF-κB,肾组织HE,PAS染色比较各组肾小球系膜增生与间质小动脉的硬化情况。结果 1.肾小球系膜增生与间质小动脉的硬化糖尿病组〉灯盏花组〉正常组,（P〈0.01）;2.肾组织NF-κB,血TGF-β1、肌酐和尿素氮水平为糖尿病组〉灯盏花组〉正常组,（P〈0.01）。结论高血糖可促进糖尿病大鼠肾脏肥大、肾小球系膜增生和间质小动脉硬化,影响肾功能。灯盏花素可通过对肾组织NF-κB及TGF-β1表达的影响,抑制糖尿病大鼠肾脏肥大、肾小球系膜增生和间质小动脉硬化,发挥保护肾功能。

Experimental study on effect of Erigeron breviscapus on the renal interstitial arteriole in diabetic rats

Objective To investigate the effect of Erigeron breviscapine on the renal interstitial arteriole in diabetic rats.Methods 70 normal male rats were selected and randomly divided into three groups：normal group（C） 20,diabetic group（A）25,breviscapine treatment group（B）25.The rat models of the diabetic nephropathy were induced by injection streptozotocin（STZ）.Erigeron breviscapine was injected into rats in group B by the coeliac cavity（20mg·kg-1·d-1）.The same amount of normal saline was injected into rats in group A and C by the coeliac cavity.Rats in three groups were killed after 2 weeks and 6 weeks of giving medicine.The blood was collected to examine serum TGF-β1,creatinine（Cre）and urea nitrogen（Bun）.Rat renal tissue was also collected to examine NF-κB.The glomerular membranoproliferation and the renal interstitial arteriolosclerosis were by the dyeing of HE and PAS.Results 1.The glomerular membranoproliferation and the renal interstitial arteriolosclerosis were in group ABC（P0.01）;2.The NF-κB in nephridial tissue,and serum level of TGF--β1,Cre and Bun were in group ABC（P0.01）.Conclusion In diabetic rats,the hyperglycaemia may increase the glomerulopathy including the glomerular membranoproliferation and the renal interstitial arteriolosclerosis,and affect the renal function.Breviscapine has renal protection on diabetic nephropathy by inhibiting the glomerular membranoproliferation and the renal interstitial arteriolosclerosis due to regulating the expression of NF-κB and TGF-β1.