改良MP法对局灶性IR脑损伤保护机制的研究.docVIP

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  • 2020-11-07 发布于浙江
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改良MP法对局灶性IR脑损伤保护机制的研究.doc

改良MP法对局灶性I/R脑损伤保护机制的研究* 梁珊1 高小平1何畔1 (1湖南师范大学附属第一医院湖南省人民医院, 湖南 长沙 410005) [摘要]:【目的】建立单侧大鼠局灶性脑缺血/再灌注(I/R)损伤模型,研究改良MP法对局灶性I/R损伤影响的可能机制。【方法】 72只SD 大鼠建立局灶性I/R模型,随机分成假手术组(SH组,n=24)、脑缺血/ 再灌注组(I/R组,n=24只)、大剂量甲基强的松龙组(MP组,n=24 只),每组根据再灌注时间点不同又分6 h、1 d、3 d、5 d 4个亚组,每组6只。在预定时间点行开阔法行为学检查,用TUNEL法和免疫组织化学方法对各组大鼠脑缺血中心及周围区神经细胞的凋亡和热休克蛋白(HSP27)、细胞色素C-3(Cyt-3)、Caspase-9 蛋白表达进行检测。【结果】 与I/R组相比, MP组可显著减少SD 大鼠探索活动;凋亡检测结果显示,MP组凋亡细胞数明显减少;免疫组织化学检测结果显示,MP组可进一步诱导HSP27蛋白表达并抑制Cyt-3 ,Caspase-9 蛋白的表达,以上P 均0.01。【结论】MP对脑I/R损伤有保护作用,调控HSP27、Cyt-3、和Caspase-9 的表达可能是其作用机制之一。 [关键词]:脑缺血; 再灌注; 甲基强的松龙 Protective mechanism of high dose of methylprednisolone for focal cerebral ischamic/reperfusion damage in rats LIANG Shan1, Gao xiao -ping1,HE pan1 (1 Clinical institute of medicine,Hunan provincial people’s hospital, 410005, Changsha , [Abstract]【Objective】To establish the damage model of focal cerebral ischamic/ reperfusion(I/R) at one side of the brain in rats and to study the possible mechanism of methylprednisolone(MP) effects towards folal cerebral ischamic/reperfusion damage. 【Methods】72 SD rats were operated to establish focal cerebral I/R model and were divided into 3 groups randomly: sham group(SH group,n=24); cerebral ischamic/reperfusion group (I/R group,n=24),treatment of MP group(MP *基金项目:湖南省卫生厅重点资助项目(2008sk3045) 作者简介:梁珊(1982-),女,医学硕士,医师,主要研究方向:临床病理学研究. E-mail:liangshan5460@126. com. TELgroup,n=24).All these 3 group were divided into 4 maller groups (6 h, 1d, 3d,5d group) according to the different observation time. Open field test was used to examine the behavioral changes, TUNEL and immunohistoch were used to observe opopsis of neuronal cells at the central and around the focal cerebral ischemia and to detect the exoression of protein HSP27、Cyt-3、Caspase-9.【Results】 The behavioral mark and the number of apoptosis neurons at the central and around the focal cerebral ischemia were much less in MP group than that in I/R group, and the expression of Hsp27 was increased and Cyt-3、Caspas

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