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作 者:王爱珍[1] 张振宇[1] 张元明[1] 郭锡熔[2] 李述庭[2]
机构地区:[1]泰州市中医院儿科,江苏泰州225300 [2]南京医科大学儿科研究所,南京210029
出 处:《实用儿科临床杂志》2007年第12期923-924,935,共3页Journal of Applied Clinical Pediatrics
基 金:江苏省教委自然科学基金项目资助(98KJD320006)
摘 要:目的探讨新生大鼠缺氧缺血性脑损伤(HIBD)后细胞凋亡抑制蛋白1(cIAP1)基因表达、Caspase-3活性的变化及地塞米松(DEX)对其影响,阐明DEX预处理对HIBD神经保护的可能机制。方法7日龄SD大鼠24只,随机分成DEX组、9g/L盐水组(NS组)、HIBD组、健康对照组。DEX、NS、HIBD组大鼠采用Rice方法制备HIBD模型。DEX和NS组在缺氧缺血前12h腹腔内分别注射DEX、等量9g/L盐水。取HIBD动物模型实验侧大脑半球,采用逆转录-聚合酶链反应(RT-PCR)检测cIAP1基因表达,比色法测定Caspase-3活性。结果与健康对照组比较,HIBD组大鼠cIAP1基因表达明显下降(P<0.01),Caspase-3活性明显上升(P<0.01)。与HIBD组比较,DEX组cIAP1基因表达明显上升,而Caspase-3活性明显下降。结论脑缺氧缺血可导致cIAP1基因表达下调,Caspase-3活性升高。DEX能通过上调cIAP1基因表达,抑制Caspase-3活性,抑制细胞凋亡,起到神经保护作用。Objective To explore the cellular inhibitor of apoptosis protein 1 ( cIAP1 ) gene expression and Caspasc - 3 activity m brain after cerebral hypoxia -ischenmia in neonatal rats and the influence of dexamethasone (DEX) on cIAP1 gene expression and Caspase -3 activity, so as to elucidate the possible mechanism of the neuro - protective effect of DEX pretreatment on rats following cerebral hypoxia - ischemia. Methods Twenty - four SD neonatal rats were divided randomly into hypoxic - ischemic brain damage group ( HIBD group), normal group (NS group) ,dexamethasone - pretreated group (DEX group) and 9 g/L NaCI control group( NS group). The animal models of HIBD were made. Total BNA from ipsilateral cerebral hemisphere was extracted. Reverse transcription polymerase chain reaction( RT - PCB) was used to evaluate the level of cIAP1 gene expression after hypoxia - ischemia. Caspase - 3 relative activity of brain tissue was determined by colorimetric assay. Results The levels of cIAP1 mBNA were lower in HIBD group than those in NS group. Caspasc - 3 relative activity significantly increased in HIBD group ( P 〈0.01 ). The levels of cIAP1 mRNA significantly increased in DEX group compared with NS group. Caspase - 3 re- lative activity significantly decreased in DEX group compared with NS group. Conclusions Cerebral hypoxia - ischemia can induce significant decrease of cIAP1 mRNA and increase of Caspase - 3 activity. By raising the expression of cIAP1 mRNA and lowering of Caspase - 3 activity, DEX may confer protection against cell death after hypoxia - ischemia in neonatal rats.
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