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目的:探讨脉络宁注射液对大鼠脑缺血再灌注(ischemia/reperfusion,I/R)损伤的保护作用及其机制。方法:健康成年雄性Sprague-Dawley(SD)大鼠随机分为假手术组、模型组、依达拉奉对照组(3 mg·kg~(-1))、脉络宁高、中、低剂量组(4,2,1 mL·kg~(-1)),每组10只,尾静脉注射给药。采用线栓法阻断大脑中动脉(middle cerebral artery occlusion,MCAO)建立大鼠I/R模型。缺血2 h,再灌注24 h时后,HE染色观察大鼠缺血侧脑组织神经血管单元(neurovascular unit,NVU)的病理变化,免疫组织化学法检测胶质纤维酸性蛋白(glialfibrillary acidic protein,GFAP)及离子钙接头蛋白(ionized calcium binding adaptor molecule 1,Iba1)的表达,蛋白免疫印记法检测肿瘤坏死因子-α(tumornecrosis factor-α,TNF-α)、白细胞介素-1β(interleukin1β,IL-1β)、血管细胞黏附分子-l(vascular cell adhesion molecule-1,VCAM-1)、细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)的表达。结果:脉络宁注射液明显改善缺血再灌注大鼠脑组织NVU的病理变化;减少GFAP和Iba1阳性细胞的数量;显著降低缺血再灌注大鼠脑组织TNF-α,IL-1β,ICAM-1,VCAM-1的表达。结论:脉络宁注射液对脑缺血再灌注大鼠神经血管单元具有明显的保护作用,其机制可能涉及抑制星形胶质细胞和小胶质细胞的激活,以及多种炎性因子的分泌和表达。
Objective: To explore the protective effect and mechanism of Mailuoning Injection on cerebral ischemia-reperfusion (I / R) injury in rats. Methods: Healthy adult male Sprague-Dawley rats were randomly divided into sham operation group, model group, Edaravone control group (3 mg · kg -1), Mailuoning high, medium and low dose groups (4,2,1 mL · kg -1), 10 rats in each group. The rat I / R model was established by occluding middle cerebral artery occlusion (MCAO) by thread occlusion. After 2 h of ischemia and 24 h of reperfusion, the pathological changes of neurovascular unit (NVU) in the ischemic brain tissue were observed by HE staining. The expressions of glial fibrillary acidic protein (GFAP) and ionized calcium binding adapter molecule 1 (Iba1) were detected by Western blot. The expressions of tumor necrosis factor-α (TNF-α), interleukin1β (IL- 1β), and the expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Results: Mailuoning injection significantly improved the pathological changes of NVU in brain tissue of ischemia-reperfusion rats, decreased the number of GFAP and Iba1 positive cells, and significantly reduced the levels of TNF-α, IL-1β, ICAM- 1, VCAM-1 expression. Conclusion: Mailuoning injection has a significant protective effect on neurovascular units in rats with cerebral ischemia / reperfusion. The mechanism may be related to the inhibition of the activation of astrocytes and microglia, as well as the secretion of many inflammatory factors expression.