首页|木犀草素对大鼠脑缺血再灌注损伤及自体神经干细胞的影响

木犀草素对大鼠脑缺血再灌注损伤及自体神经干细胞的影响

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目的 探讨木犀草素对大鼠脑缺血再灌注损伤及自体神经干细胞的影响.方法 将40只SD大鼠随机分为5组,分别为模型组、假手术组以及木犀草素高、低2个剂量组,其中高剂量给予50 mg/kg的木犀草素,低剂量组给予10 mg/kg的木犀草素.连续给药7 d,在末次给药1 h后,对颈总动脉进行结扎处理以复制脑缺血再灌注损伤模型;测定各组大鼠脑组织中IL-10、IL-1β和TNF-α含量,利用TTC染色法对各组大鼠脑梗死百分比进行测定并对大鼠的神经功能进行分析;采用免疫组化方法测定各组大鼠脑组织中BrdU+和Nestin+的数量.结果 与模型组比较,木犀草素能改善大鼠的神经功能,降低大鼠脑梗死百分比(P<0.05);同时木犀草素能够大幅降低脑组织中IL-1β和TNF-α的含量(P<0.05),提高脑组织中IL-10的含量(P<0.05),并显著提高大鼠脑组织中BrdU+和Nestin+的数量(P<0.05).结论 木犀草能够显著改善缺血再灌注大鼠脑损伤程度,同时还能够提高自体神经干细胞的含量.
Luteolin protects brain injury and improves endogenous neural stem cells proliferation on cerebral ischemia-reperfusion injury in rat
Objective To investigate the protective effects of luteolin on cerebral ischemia-reperfusion injury in rats.Methods 40 SD rats were randomly divided into four groups:sham group,model group,luteolin low and high dose groups.Each group was given oral administration for 7 days.After 1 h of last administration,the CIRI ( cerebral ischemia-reperfusion injury) group was produced inserting 5-0 line into the internal carotid artery.Then levels of IL-10, IL-1βand TNF-αcontents in myocardial tissues were measured.Meanwhile,infarct size was detected by TTC staining and number of BrdU +and Nestin + were measured by immunohistochemical methods.Results Compared with model group, luteolin could significantly decrease the levels of TNF-αand IL-1βin cerebral tissues(P<0.05),improve IL-10 content in cerebral tissues(P<0.05),and effectively reduce myocardial infarct range(P<0.05).Meanwhile luteolin could improve the expressions of BrdU + and Nestin + in cerebral tissues(P <0.05).Conclusion Luteolin has beneficial effects on rats with cerebral ischemia-reperfusion injury and improves endogenous neural stem cells proliferation.

luteolincerebral ischemia-reperfusionendogenous neural stem cells

肖婷婷、帕力达·克立木、余丹

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中南大学湘雅医学院附属海口医院神经内科,海南海口570208

新疆维吾尔自治区人民医院神经内科,新疆乌鲁木齐830001

木犀草素 脑缺血再灌注 自体神经干细胞

海南省重点科技计划应用研究及产业化项目

ZDXM20130066

2017

中国生化药物杂志
南京生物化学制药研究所,全国生化制药情报中心站,中国生化制药工业协会,中国药品生物制品检定所

中国生化药物杂志

ISSN:1005-1678
年,卷(期):2017.37(3)
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