Zhongguo cuzhong zazhi (Apr 2018)
群多普利对大鼠脑缺血再灌注损伤的保护作用研究 Neuroprotective Effects of Trandolapril on Rat Cerebral Ischemia-reperfusion Injury
Abstract
目的 观察群多普利对大鼠局灶性脑缺血损伤的保护作用，并探究其可能作用机制。 方法 采用改良ZeaLonga's法制作大脑中动脉闭塞（middle c erebral a rtery o cclusion，MCAO）模型。将 健康雄性SD大鼠随机分成假手术组、模型组、群多普利低剂量组（5 mg/kg）、群多普利高剂量组 （10 mg/kg）等四组，观察各实验组大鼠神经功能评分、脑梗死体积、脑组织白细胞介素（i nterl euki n， IL）-1β及IL-10含量变化。 结果 与假手术相比，模型组神经功能缺损程度评分显著提高，脑组织IL-1β及IL-10含量显著增加 （P＜0.05）；与模型组比较，群多普利低剂量和高剂量均能显著减轻缺血再灌注损伤大鼠神经功能 缺损，减小脑梗死体积（P＜0.05）；群多普利低剂量和高剂量均能显著降低IL-1β的含量；群多普利 高剂量可进一步增加IL-10的含量。 结论 在脑缺血再灌注损伤大鼠中，群多普利可能通过调节IL-1β及IL-10的分泌，重建促炎因子与抗 炎因子之间的平衡，从而起到神经保护作用。 Abstract: Objective To investigate the neuroprotective effect of Trandolapril on cerebral ischemiareperfusion injury, and explore its possible mechanism. Methods The model of focal ischemic reperfusion in Sprague-dawley (SD) rats was prepared by middle cerebral artery occlusion (MACO) with a nylon monofilament suture. Adult male SD rats were divided randomly into sham operation group, model group, and Trandolapril treatment groups (low dosage 5 mg/kg, high dosage 10 mg/kg). The changes of neurological function scores, the cerebral infarction volumes, interleukin (IL)-1β and IL-10 content in the brain were observed. Results Compared with the sham group, integrals of neurologic defect degree, infarction volume and the IL-1β and IL-10 content in the brain of the model group were significant increased (P <0.05). Compared with the model group, treatment with Trandolapril (5 mg/kg and 10 mg/kg) lowered the integrals of neurologic defect degree and reduced the cerebral infarction volumes. Trandolapril (5 mg/kg and 10 mg/kg) could significantly reduce the content of IL-1β (P <0.05), and Trandolapril (10 mg/kg) could significantly increase the content of IL-10. Conclusion Trandolapril could alleviate cerebral ischemia reperfusion injury by regulating the expression of the pro-inflammatory IL-1β and anti-inflammatory IL-10 cytokines.
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