丁苯酞对缺血性脑卒中大鼠脂联素、MCP-1及slCAM-1的影响

目的:探讨丁苯酚对卒中大鼠脂联素、MCP-1和sl CAM-1表达的影响。方法:建立大鼠永久性大脑中动脉梗塞(Permanent middle cerebral occlusion, pMCAO)局灶性脑缺血模型,将SD大鼠分为Sham组、pMCAO模型组和NBP治疗组;甲酚紫染色法测定大鼠脑部梗塞面积;改良神经功能损害评分(Modified neurological severity score, m NSS)用于评定各组大鼠的神经功能变化情况;Elisa法检测大鼠脑部和血清中脂联素水平以及脑部MCP-1和sl CAM-1水平。结果:药物处理后pMCAO组大鼠存活率明显低于Sham组;NBP处理能够有效逆转pMCAO诱导的大鼠m NSS得分的升高;与Sham组相比,pMCAO组大鼠脑部梗塞面积显著增加,NBP处理明显减少了损伤大鼠的梗塞范围;与Sham组相比,p MCAO组大鼠脑部和血清中脂联素表达明显降低,而大脑MCP-1及sl CAM-1水平显著升高,NBP处理上调了大脑和血清脂联素的水平并抑制脑部MCP-1和sl CAM-1的表达。结论:丁苯酞通过上调脂联素表达,抑制MCP-1及sl CAM-1的水平对缺血性脑卒中大鼠起到神经保护作用。

Effects of Butylphthalide on Adiponectin, MCP-1 and slCAM-1 after Ischemic Stroke in Rats

ABSTRACT Objective: To investigate the effects of butylphthalide on the expression of adiponectin, MCP-1 and slCAM-1 after stroke in rats. Methods: A rat model of permanent middle cerebral occlusion (pMCAO) was established. The SD rats were divided into Sham group, pMCAO model group and NBP treatment group; Brain infarct size in rats was determined by cresyl violet staining; Modified neurological severity score (mNSS) was used to assess changes in neurological function in each group of rats; Elisa method for detecting adiponectin levels in brain and serum of rats and levels of MCP-1 and slCAM-1 in the brain. Results: The survival rate of pMCAO group was significantly lower than that of sham group after the drug treatment; NBP treatment could effectively reverse the increase of pNSAO-induced mNSS score in rats; Compared with Sham group, the brain infarct size of pMCAO group was significantly increased, NBP Treatment significantly reduced the infarct size of injured rats; Compared with Sham group, the expression of adiponectin in brain and serum of pMCAO group was significantly decreased, while the levels of MCP-1 and slCAM-1 in brain were significantly increased, and NBP treatment up-regulated the levels of brain and serum adiponectin and inhibited the expression of MCP-1 and slCAM-1 in the brain. Conclusion: Butylphthalide exerted neuroprotective effects on ischemic stroke rats by up-regulating the expression of adiponectin and inhibiting the levels of MCP-1 and slCAM-1.