摘要
目的 :了解中药糖复康治疗糖尿病肾病 (DN)的机制。方法 :应用链尿佐菌素糖尿病大鼠模型 ,用免疫组化S P法检测糖尿病大鼠肾皮质蛋白质非酶糖化终产物 (AGES) ,细胞间粘附分子 1(ICAM 1) ,Ⅳ型胶原 (Ⅳ C) ,纤维连接蛋白 (FN) ;放射免疫法检测血中白细胞介素 1β(IL 1β) ;ELISA法检测血中肿瘤坏死因子 α(TNF α) ,并与蛋白质非酶糖化终产物AGES 生成抑制剂氨基胍作对照 ,分析中药糖复康对早期DN大鼠蛋白质非酶糖化、炎性细胞因子的影响。结果 :糖复康和氨基胍均显著下调了AGES的表达 ,但下调炎性因子ICAM 1,IL 1β ,TNF α及细胞外基质成分Ⅳ C ,FN的表达 ,则糖复康明显优于氨基胍。结论 :抑制糖尿病时蛋白质非酶糖基化 ,下调炎性因子表达 ,可能是糖复康治疗DN的部分机制 。
Objective: To find out the mechanism of Tangfukang on the diabetic nephropathy(DN). Method: A Model of streptorotocin diabetic rats was used. The expressions of the AGE s, ICAM 1, IV C and FN were observed in renal cortex of diabetic rats with immunohistochemical method. The level of the IL 1β in blood serum was measured by radioimmunoassay method and the level of TNF was determined in blood serum by ELISA method. Aminoguanidine was selected as the control medicine which could inhibit the expression of monenzymatic glycosylation end products of protein. All the results were compared to analyze the effect of Tangfukang on monenzymatic glycosylation of protein and cytokine expression in early diabetic nephropathy rats. Result: Both Tangfukang and aminoguanidine significantly decreased the expression of AGE S, but Tangfukang was greatly superior to aminoguanidine in suppressing the expression of cytokine like ICAM 1, IL 1β, TNF α and the ingredients of extracellular matrix like Ⅳ C, FN. Conclusion: It may be the partical mechanism of Tangfukang to suppress the monenzymatic glycosylation of protein and to reduce the expression of cytokine in diabetes. The effect of Tangfukang is superior to that of aminoguanidine.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2003年第5期452-455,共4页
China Journal of Chinese Materia Medica
基金
天津市自然基金课题 (973 60 90 11)