芒果苷对自发性高血压大鼠脑组织炎症损伤的保护作用

摘要

目的 观察芒果苷mangiferin对自发性高血压大鼠脑组织炎症损伤的保护作用以及对脑组织炎性因子表达MCP-1/CCR2信号通路的影响.方法 40只自发性高血压大鼠随机分为模型组,苯那普利组[10 mg/(kg-d)]与芒果苷高、中、低剂量[40、20、10 mg/(kg·d)]组,另外8只同周龄的雄性大鼠为正常对照组.连灌胃给药8周后,观察自发性高血压大鼠的脑组织形态学;用ELISA法测定大鼠脑组织中肿瘤坏死因子TNF-α、白细胞介素IL-6、细胞间粘附分子ICAM-1的水平;免疫组织化学法和Western blot法检测大鼠脑组织单核细胞趋化蛋白MCP-1、细胞表面趋化因子受体CCR2蛋白的表达,RT-PCR检测大鼠脑组织MCP-1、CCR2 mRNA的表达.结果 正常对照组及模型组脑组织形态学均无明显病变,苯那普利组、芒果苷各剂量组形态学均正常.芒果苷可显著降低自发性高血压大鼠脑组织IL-6、TNF-α、ICAM-1的含有量及MCP-1、CCR2蛋白和mRNA表达量.结论 芒果苷对自发性高血压大鼠脑组织的炎症具有明显的抗炎作用,其机制与抑制MCP/CCR2信号通路表达有关.%AIM To observe the protective effects of mangiferin on the inflammatory injury and expression of the inflammatory factor in the cerebral tissue of spontaneously hypertensive rats and on MCP-1/CCR2 signal pathway.METHODS Forty spontaneously hypertensive rats were randomly divided into model,benazepril [10 mg/(kg · d)] and mangiferin high,middle and low dose [40,20,10 mg/(kg · d)] groups and other eight rats of same week age served as control group.After consecutive intragastric administration for eight weeks,morphology of the rats' cerebral tissue was observed;their levels of ICAM-1,IL-6 and TNF-α in cerebral tissue were determined by ELISA;their expressions of MCP-1 and CCR2 protein in brain tissue of rats were detected by immunohistochemistry and Western blot and the detection of mRNA expressions of MCP-1 and CCR2 in cerebral tissue of rats were carried out by RT-PCR.RESULTS Compared with the model group,the blood pressure of mangiferin in each dosage group decreased slightly,but there was no significant statistical difference.In the control group and the model group,there was no obvious morphological change in the cerebral tissue.The morphology of rats in the benazepril group,each dose of mangiferin group were all normal.The contents of IL-6,TNF-α,ICAM-1 and MCP1,CCR2 protein and mRNA expression were significantly decreased in the cerebral tissues of spontaneously hypertensive rats.CONCLUSION Mangiferin has obvious anti-inflammatory effects on inflammatory reaction in spontaneously hypertensive rats,its mechanism may be related to inhibiting the expression of MCP/CCR2 signaling pathway.