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目的观察解聚复肾宁(Jiejufushenning,JJFSN)对糖尿病(Diabetes mellitus,DM)大鼠肾组织肿瘤坏死因子-α(Tumor necrosisfactor-alpha,TNF-α)、单核细胞趋化蛋白-1(Monocyte chemoattractant protein-1,MCP-1)和血清TNF-α的影响,探讨其肾保护作用机制。方法腹腔注射链脲佐菌素(Streptozotocin,STZ)建立SD大鼠DM模型,将成模DM大鼠随机分为3组:DM模型组(B组)、JJFSN组(C组)、厄贝沙坦(Irbesartan)组(D组),另设正常对照组(A组)。采用相应干预措施处理12周。常规方法测定12周末各组大鼠空腹血糖(FBG)、血尿素氮(BUN)、血肌酐(Scr)、肾重/体重(KW/BW)、24 h尿蛋白(24 huPro);放免法测血清TNF-α含量;免疫组织化学方法测肾组织TNF-α、MCP-1的表达;PAS染色评估细胞外基质;电镜观察肾组织超微结构改变。结果与A组相比,B组大鼠FBG、BUN、Scr、KW/BW、24 huPro及血清TNF-α升高(P<0.05),肾组织TNF-α、MCP-1表达明显增高(P<0.05);肾组织超微结构明显异常;C组和D组上述指标显著改善(P<0.05),肾组织超微结构异常改善。结论JJFSN能延缓DM大鼠肾损害进程,其机制可能与抑制TNF-α、MCP-1上调有关。
Objective To observe the effects of Jiejufushenning (JJFSN) on the expression of Tumor necrosis factor-α (TNF-α) and Monocyte chemotactic protein-1 (Monocyte) in Diabetes mellitus (DM) chemoattractant protein-1, MCP-1) and serum TNF-α, to explore its mechanism of renal protection. Methods DM model of SD rats was established by intraperitoneal injection of Streptozotocin (STZ). DM model rats were randomly divided into three groups: DM model group (B), JJFSN group (C), irbesartan (Irbesartan) group (D group), another normal control group (A group). The corresponding interventions for 12 weeks. The fasting blood glucose (FBG), blood urea nitrogen (BUN), serum creatinine (Scr), kidney weight / body weight (KW / BW) and 24 h urinary protein The content of TNF-α in serum was measured. The expression of TNF-α and MCP-1 in renal tissue was detected by immunohistochemical method. The extracellular matrix was evaluated by PAS staining. The ultrastructure of renal tissue was observed by electron microscope. Results Compared with group A, the levels of FBG, BUN, Scr, KW / BW, 24 huPro and serum TNF-α in group B were significantly increased (P <0.05) <0.05). The ultrastructure of renal tissue was obviously abnormal. The above indexes in group C and group D were significantly improved (P <0.05), and the ultrastructure of renal tissue was improved. Conclusion JJFSN can delay the process of renal damage in DM rats, which may be related to the upregulation of TNF-α and MCP-1.