Neuroprotective effect and mechanism of Mu-Xiang-You-Fang on cerebral ischemia-reperfusion injury in rats.
Neuroprotective effect and mechanism of Mu-Xiang-You-Fang on cerebral ischemia-reperfusion injury in rats.
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DOI：
10.1016/j.jep.2016.07.016
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发表时间：
2016-11
影响因子：
5.4
通讯作者：
Qipeng Zhao;Xiuli Cheng;Xiaobo Wang;Jing Wang;Yafei Zhu;Xueqin Ma
中科院分区：
文献类型：
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作者：
Qipeng Zhao;Xiuli Cheng;Xiaobo Wang;Jing Wang;Yafei Zhu;Xueqin Ma
本研究旨在探讨木香攸方（MXYF）对脑缺血再灌注（I/R）损伤的神经保护作用及其相关信号通路。假手术组、缺血再灌注组、尼莫地平组和MXYF组（分别为58、116和232 mg/kg）。采用大脑中动脉阻断2 h再灌注48 h的方法建立脑缺血模型。再灌注48 h后，采用Zea longa评分法进行神经功能评分，TTC染色法测定脑梗死面积。Western blot检测细胞色素c（cyt-c）、Bcl-2、Bax、caspase-9、caspase-3、caspase-7蛋白表达;采用逆转录-聚合酶链反应（RT-PCR）检测Caspase-3、Caspase-7的表达。（116和232 mg/kg）显著降低神经功能评分，缩小脑梗死面积。Western blot分析显示，MXYF（116和232 mg/kg）处理后，Bcl-2表达增强，Bax表达受到抑制，Bcl-2/Bax比值显著升高。细胞色素c、caspase-9、caspase-3和caspase-7蛋白表达明显受到抑制，而caspase-9、caspase-3和caspase-7 mRNA表达明显受到抑制。caspase-3和caspase-7在MXYF中被显著抑制，而cyt-c在MXYF中未被显著抑制（116和232 mg/kg）治疗组与I/R组比较。结论上述数据表明，MXYF具有潜在的神经保护作用，通过调节细胞凋亡途径，MXYF是一种很有前途的治疗中风的药物。
Ethnopharmacological relevanceThe present study is to investigate the neuroprotective effect of Mu-Xiang-You-Fang (MXYF), a classic Traditional Chinese Medicine used by Chinese minorities to treat stroke, on cerebral ischemia-reperfusion (I/R) injury and the related signaling pathways.Materials and methodsMale Sprague-Dawley rats were divided into 6 groups: sham group, I/R group, nimodipine and MXYF (58, 116 and 232 mg/kg respectively) groups. Cerebral ischemia model was induced by middle cerebral artery occlusion for 2 h followed by reperfusion for 48 h. Neurological functional score was evaluated according to the method of Zea longa’s score and the infarct area was determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining at 48 h after reperfusion. The protein expression of cytochrome c (cyt-c), Bcl-2, Bax, caspase-9, caspase-3 and caspase-7 were analyzed by western blot and the mRNA expression of Caspase-9, Caspase-3 and Caspase-7 were determined by the reverse transcription-polymerase chain reaction.ResultsOral administration of MXYF (116 and 232 mg/kg) significantly reduced the neurological functional score and attenuated the cerebral infarct area. Western blot analysis showed that the expression of Bcl-2 is enhanced and Bax expression is inhibited after treatment with MXYF (116 and 232 mg/kg), leading to significant increase of the ratio between Bcl-2 and Bax. Furthermore, the protein expression of cyt-c, caspase-9, caspase-3 and caspase-7 was significantly inhibited while the mRNA expression of caspase-9, caspase-3 and caspase-7 but not cyt-c was markedly inhibited in the MXYF (116 and 232 mg/kg) treatment groups compared with the I/R group.ConclusionsThe above data suggested that MXYF has potential neuroprotective activities by the regulation of apoptotic pathway, MXYF is a promising agent in treatment of stroke.