参芪复方对GK大鼠炎症标志物的影响及机理探讨

目的:探讨参芪复方对2型糖尿病(type 2 d iabetes m ellitus,T2DM)炎症标志物的影响及作用机理。方法:设模型、雷米普利(1 mg/kg.d)、参芪复方低、高剂量(0.72 g/kg.d与2.88 g/kg.d)及W istar对照组,各组动物每天灌胃相应受试物32 d。酶免法检测血清C反-应蛋白(C-reactive prote in,CRP)、放免法检测血清肿瘤坏死因子(tumour necrosis factor,TNFα)-含量;实时定量RT-PCR和免疫组织化学法分别检测主动脉核因子(NF)κ-B p65mRNA的表达和活化。结果:参芪复方低、高剂量组CRP、TNFα-含量均显著低于模型组(P<0.05或P<0.01),NFκ-B p65表达与活化均降低(P<0.05或P<0.01)。结论:参芪复方具有降低T2DM血清炎症标志物水平的作用,减少NFκ-B基因的表达和活化可能是其作用机理之一。

Effects and Mechanism of ShenQi Compound Recipe on Inflammation Maker in GK Rats

OBJECTIVE: To explore the effects and mechanism of ShenQi Compound Recipe on inflammation maker of type 2 diabetes mellitus in GK rats. METHODS: Rats were ranodmly divided into Model group, Ramipril group (positive control, 1 mg/kg x d), SQCR low dosage (0.72 g/kg x d), SQCR high dosage group (2.88 g/kg x d) and Wistar control group. Each group was administrated correspondent substance respectively for 32 days. Determined C-reactive protein (CRP) by ELISA and tumour necrosis factor (TNF)-alpha by radioimmunassay. The mRNA expression of nuclear factor (NF)-kappaB p65 in aorta was determined by real time RT-PCR, and activation of it using immunohistochemistry staining. RESULTS: Concentrations of CRP and TNF-alpha in serum and the expression of mRNA and activation of NF-kappaB were all decreased in SQCR low and high dosage groups compared with model group (P < 0.05 or P < 0.01). CONCLUSION: These results suggest that SQCR can decrease the level of inflammation maker in serum, which may be resulted from reducing the mRNA expression and activation of NF-kappaB.