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作 者:汪兴宇[1] 张宇燕[1] 万海同[1] 赵涛 付巍 周惠芬[1] 周鹏[1] 王泽锋[1] 杨洁红
机构地区:[1]浙江中医药大学心脑血管病研究所,浙江杭州310053 [2]山东步长制药有限公司,山东菏泽274000
出 处:《中国中药杂志》2014年第3期503-506,共4页China Journal of Chinese Materia Medica
基 金:国家自然科学基金项目(81173647;81202636;81274176);浙江省自然科学基金项目(LR12H27001);浙江省卫生高层次创新人才培养工程项目;浙江省中医药(中西医结合)重点学科项目(2012-XK-A06)
摘 要:目的:研究参芎注射液对老龄大鼠脑缺血再灌注损伤的保护作用。方法:108只SD大鼠随机分为假手术组、模型组、尼莫通组、参芎注射液高、中、低剂量组(36.4,18.2,9.1 mL·kg-1·d-1)。采用线栓法建立大鼠脑缺血再灌注模型,观察参芎注射液对脑缺血再灌注损伤大鼠的神经功能评分、脑梗死体积的影响,检测脑组织中一氧化氮合酶(NOS)、一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)、乳酸脱氢酶(LDH)的含量,ELISA法检测对脑组织中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)水平的影响。结果:参芎注射液可显著降低脑缺血再灌注大鼠的神经功能评分,减轻脑组织损伤程度,减少脑梗死范围,提高SOD活力,降低MDA,NO,NOS,LDH水平,抑制IL-1β和TNF-α的表达。结论:参芎注射液对大鼠缺血再灌注损伤具有明显的保护作用,其机制可能与改善神经功能、减少自由基损伤和抑制炎症因子表达有关。Objective: To study the protective effect of Shenxiong injection on the cerebral ischemia-reperfusion injury of senile rats. Method: Totally 108 Sprague-Dawley (SD) rats were randomly divided into the sham operation group, the model group, the Nimodipine group and Shenxiong injection groups (low, middle, and high doses). The rat brain ischemia-reperfusion model was established by the middle cerebral artery occlusion (MCAO) method in rats, in order to observe the effect of Shenxiong injection on neurological score and brain infarct volume of rats with cerebral ischemia-reperfusion injury, and determine the contents of NOS, NO, SOD, MDA and LDH in brain tissues. The contents of TNF-a and IL-1β levels in brain tissues were measured by enzyme-linked immunosorbent assay (ELISA) method. Result: Shenxiong injection could significantly decrease neurological score, injury degree of brain tissues and brain infarct volume of rats with cerebral ischemia-reperfusion injury, increase the vigor of SOD, decrease the levels of MDA, NO, NOS and LDH, and inhibit IL-1β and TNF-a expressions. Conclusion: Shenxiong injection has the obvious protective effect on the brain ischemia-reperfusion injury in rats. Its mechanism may be related to the improvement of neurological function, the reduction of free radical injury, and the inhibition of inflammation factor expression.
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