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目的观察姜黄素对糖尿病脑病大鼠胰岛素样生长因子1(IGF-1)、胰岛素样生长因子受体(IGF-1R)表达的影响,分析姜黄素的脑保护作用机制。方法实验动物分为4组:正常对照组(A组)、正常姜黄素组(B组)、糖尿病脑病组(C组)和姜黄素治疗组(D组)。以大鼠一次性腹腔注射链脲佐菌素(STZ)建立糖尿病脑病模型,姜黄素持续灌胃12周。观察大鼠的体质量、血糖、糖化血红蛋白变化,采用免疫组化、RT-PCR法检测IGF-1及IGF-1R表达的变化。结果与A组和B组大鼠相比,C组大鼠血糖、糖化血红蛋白明显增高,体质量下降,海马区IGF-1表达明显减少(P<0.05),同样海马神经元IGF-1R表达减少(P<0.05)。经姜黄素治疗后,D组大鼠糖化血红蛋白下降,体质量增加,血糖变化不大,海马神经元IGF-1表达增多(P<0.05),随之海马神经元IGF-1R表达增多(P<0.05)。结论大鼠海马IGF-1/IGF-1R表达的减少可能在糖尿病脑病发病机制中发挥着重要的作用,姜黄素有脑保护作用,其机制可能是通过调控IGF-1信号通路调节实现的。
Objective To observe the effect of curcumin on the expression of insulin-like growth factor 1 (IGF-1) and insulin-like growth factor receptor (IGF-1R) in diabetic encephalopathy rats and to analyze the protective mechanism of curcumin. Methods The experimental animals were divided into 4 groups: normal control group (A group), normal curcumin group (B group), diabetic encephalopathy group (C group) and curcumin treatment group (D group). A rat model of diabetic encephalopathy was established by intraperitoneal injection of streptozotocin (STZ) in rats. Curcumin was continuously intragastrically administered for 12 weeks. The changes of body weight, blood glucose and glycosylated hemoglobin were observed. The expressions of IGF-1 and IGF-1R were detected by immunohistochemistry and RT-PCR. Results Compared with group A and group B, the blood glucose and HbA1c of the rats in group C were significantly increased, the body weight was decreased, the expression of IGF-1 in hippocampus was significantly decreased (P <0.05), and the expression of IGF-1R in hippocampal neurons was also decreased (P <0.05). After treatment with curcumin, the levels of HbA1c decreased, the body weight increased, the blood glucose changed little, the expression of IGF-1 in hippocampal neurons increased (P <0.05) and the expression of IGF-1R increased in hippocampal neurons (P < 0.05). Conclusion The decrease of IGF-1 / IGF-1R expression in the hippocampus of rats may play an important role in the pathogenesis of diabetic encephalopathy. Curcumin has a protective effect on brain. Its mechanism may be through the regulation of IGF-1 signaling pathway.