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目的研究丹酚酸B(SalB)对脑缺血再灌注损伤大鼠炎症反应的干预作用。方法雄性Wistar大鼠随机分为3组:假手术组、模型组、实验组,制作脑中动脉闭塞模型(MCAO),缺血1 h再灌注。分别于大鼠苏醒后、再灌注24,48 h,实验组腹腔注射SalB(12 mg·kg-1),模型组以等体积0.9%NaCl替代。在4个时间点(6,24,48,72 h)进行神经功能缺损评分,检测外周血白细胞计数、中性粒细胞绝对值,ELISA法检测血浆C反应蛋白水平(CRP),实时荧光定量RTPCR法检测缺血侧脑组织ICAM-1、E-selectin mRNA表达。结果 SalB可以改善模型大鼠神经功能缺损症状,降低外周血白细胞计数、中性粒细胞绝对值及血浆CRP水平,抑制缺血侧脑组织ICAM-1、E-selectin mRNA表达。结论SalB具有抗脑缺血再灌注损伤作用,其机制可能与抑制损伤后整体炎症反应水平及脑组织内黏附分子的表达有关。
Objective To investigate the effect of salvianolic acid B (SalB) on the inflammatory response in rats with cerebral ischemia-reperfusion injury. Methods Male Wistar rats were randomly divided into 3 groups: sham operation group, model group and experimental group. Middle cerebral artery occlusion model (MCAO) was established and ischemia 1 h reperfusion was performed. Rats were resuscitated, reperfusion 24h, 48h, experimental group intraperitoneal SalB (12 mg · kg-1), the model group with an equal volume of 0.9% NaCl instead. Neurological deficit scores were measured at 4 time points (6, 24, 48 and 72 h). Peripheral blood leukocyte count, neutrophil absolute value, plasma C-reactive protein level (CRP), real-time fluorescent quantitative RTPCR Method to detect ICAM-1, E-selectin mRNA expression in ischemic brain. Results SalB could ameliorate the symptoms of neurological deficit, reduce the peripheral blood leukocyte count, neutrophil absolute value and plasma CRP level, and inhibit the expression of ICAM-1 and E-selectin mRNA in the ischemic brain tissue. Conclusion SalB can protect against ischemia-reperfusion injury and its mechanism may be related to the inhibition of the overall inflammatory response and the expression of intracellular adhesion molecules.