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作 者:邓顺有[1] 范萍[1] 张征 张彤[1] 吴琳英[1]
机构地区:[1]广州医学院第一附属医院内分泌科,广东广州510120 [2]广州市海珠区第二人民医院内科,广东广州510250
出 处:《中国现代医学杂志》2013年第2期36-41,共6页China Journal of Modern Medicine
基 金:广州市中医药中西医结合科研基金(No:2010A22);广州医学院博士启动项目(No:2008C28)
摘 要:目的观察活血降糖胶囊对糖尿病肾病(DN)大鼠肾组织Ⅳ型胶原(Ⅳ-C)蛋白表达及MMPs/TIMPs系统作用的影响。方法将SD雄性大鼠复制为DN动物模型,筛选DN成模大鼠,随机分成模型(DNM)组、中药(HX)组、西药(IR)组,并随机设正常对照(NC)组,分别予中西药物干预;8周后处死大鼠取肾组织,以免疫组织化学方法测定IV-C、MMP-9、MMP-2及TIMP-1、TIMP-2的蛋白表达,计算积分光密度及面密度比值。结果 HX组和IR组的Ⅳ-C免疫组织化学染色面密度及积分光密度较DNM组降低,MMP-9、MMP-2免疫组织化学染色面密度及积分光密度较DNM组升高,DNM组TIMP-1、TIMP-2与HX组和IR组比较呈强阳性表达,HX组和IR组染色面积及积分光密度均较DNM组降低,差异有统计学意义(P<0.01);MMPs/TIMPs比值与Ⅳ-C免疫组织化学染色面积呈负相关(r1=-0.929,r2=-0.908,P<0.01)。结论滋肾活血中药——活血降糖胶囊可能通过调节肾组织MMPs/TIMPs系统蛋白表达,改善Ⅳ-C代谢,延缓DN肾小球硬化进程,对DN肾脏发挥保护作用。[Objective] To investigate the expression of matrix metalloproteinases (MMPs), tissue inhibitor of metalloproteinases (TIMPs) and collagen Ⅳ (IV-C) in kidney of diabetic nephropathy rats and the intervention effect of Huoxue Jiangtang capsule with nourishing kidney and promoting blood flow. [Methods] The male SD rats were intraperitoneally to reduce diabetic nephropathy animal models. The animal models were randomly divided into three groups: diabetic nephropathy model group (DNM), medicated group treated by Huoxue Jiangtang capsule group (HX) and medicated group treated by irbesartan group (IR), and randomly assigned normal control group (NC). After 8 weeks the expression of MMPs, TIMPs and IV-C in rat model kidney tissue were detected by immunohistochemistry method (SP). [Results] Compared with DNM group, HX group and IR group showed the values of area density and photodensity of positively stained area of MMP-2 and MMP-9 significantly increased while that of TIMP-2, TIMP-1 and IV-C reduced (P〈0.01). The ratio of MMPs/TIMPs and photodensity of IV-C changed in reverse direction (r1=-0.929, r2=-0.908, P 〈0.01).[Conclusion] Huoxue Jiangtang capsule with nourishing kidney and promoting blood flow may regulate the balance of MMPs and TIMPs and weaken the accumulation of Ⅳ-C to protect kidney and ameliorate the structure and function damage of diabetic nephropathy model rats.
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