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作 者:刘雪梅[1] 黄启福[1] 张允岭[2] 柳洪胜[2] 娄金丽[2] 郑宏[2]
机构地区:[1]北京中医药大学基础医学院病理学教研室,北京100029 [2]北京中医药大学东方医院
出 处:《北京中医药大学学报》2007年第5期310-313,I0001,共5页Journal of Beijing University of Traditional Chinese Medicine
基 金:国家重点基础研究发展计划(973计划)项目(No.2006CB504805);吉林敖东洮南药业股份有限公司开发基金
摘 要:目的研究心脑舒通胶囊对局灶性脑缺血再灌注大鼠神经细胞的保护作用,并探讨其抗氧化作用。方法采用线栓法阻塞大脑中动脉致大鼠局灶性脑缺血再灌注模型(MCAO),24h后断头取脑,HE染色,光镜下观察大鼠大脑皮层区细胞损伤程度,TUNEL法检测皮层区神经细胞凋亡程度,分光光度计检测患侧脑组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、乳酸(LD)、乳酸脱氢酶(LDH)的含量。结果缺血再灌注模型组大鼠均出现明显的神经功能缺损症状,有明显缺血性形态学改变如细胞水肿等;皮层区凋亡细胞数增多,缺血侧脑组织的MDA增多、SOD活性降低,与假手术组比较均有显著性差异(P<0.01)。心脑舒通胶囊能明显改善MCAO大鼠神经症状体征,减轻皮层区神经细胞水肿,降低细胞凋亡;并可显著提高SOD活性,降低MDA、LD、LDH的含量,与模型组比较有统计学意义(P<0.05~0.01)。结论心脑舒通胶囊有减轻缺血再灌注脑组织损伤程度、降低神经细胞凋亡的作用,其机制可能是通过调整氧化应激、提高自由基酶性清除能力,从而减轻脑损伤。Objective To study the protective effect and the anti-oxidation mechanism of Xinnaoshutong Capsules on neurons in rats with focal cerebral ischemia and reperfusion. Methods Rat model of focal cerebral ischemia and reperfusion was established by thread ligation in "middle cerebral artery. After 24 hours, the morphological changes of rat cerebral cortical neurons ( HE staining) were observed under optical microscope, apoptosis of cortical neurons was detected by TUNEL, the content of MDA,SOD LD and LDH in ischemic cerebral brain were detected by spectrophotometry. Results Compared with the control group, there were obvious neurological deficits in the ischemia and reperfusion model groups. The significant iscbemic morphologic changes in cerebral cortex were observed , such as neuronal edema and amount of apoptosis neurons. The content of MDA was much higher, whereas that of SOD was much lower in ischemia cerebra ( P 〈 0. 01 ). The neurological deficits of middle cerebral artery occlusion ( MCAO) rats could be improved and the neuronal edema and neuronal apoptosis of cortex could be lessened in the Xinnaoshutong Capsules group. Compared with the control group, MDA, LD and LDH were decreaced , and SOD was increased significantly in the Xinnaoshutong Capsules group (P 〈 0. 05 0.01 ). Conclusion Xinnaoshutong Capsules have the effect of lightening the injury degree of brain tissues and decreasing neuronal apoptosis after cerebral ischemia and reperfusion. The mechanism might be related to regulating oxidative stress response and elevating the free radical scavenging capability to alleviate cerebral injury .
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