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目的研究低分子肝素(LMWH)对局部脑缺血再灌注后脑组织中NMDA受体I型亚单位(NR1) mRNA表达及细胞凋亡的影响,探讨LMWH对缺血再灌注后神经元的保护作用及可能机制。方法参照Zea Longa线栓法制作大鼠大脑中动脉阻塞模型(MCAO),140只SD大鼠被随机分成假手术组、缺血再灌组(MCAO组)和LMWH干预组。每组大鼠再随机分成4组:分别在再灌注后6h、24h、48h、96h处死。进行TUNEL染色检测缺血区细胞凋亡情况,并用原位杂交方法检测NR1 mRNA。结果MCAO组大鼠大脑皮质梗死灶的凋亡细胞和NR1 mRNA表达与假手术组比较明显增强(P<0.01),而LMWH干预组未能阻止再灌注后凋亡的发生,且阳性细胞数48h最多,与6h、24h比较有统计学意义(P<0.01),但与MCAO组比较有凋亡细胞数明显减少(P<0.01)。结论再灌注后脑组织中NR1 mRNA表达增强,与细胞凋亡密切相关。低分子肝素可能通过抑制NR1 mRNA的表达,抑制缺血半暗区的细胞凋亡。
Objective To investigate the effects of low molecular weight heparin (LMWH) on the expression of NMDA receptor subtype I (NR1) mRNA and apoptosis after focal cerebral ischemia / reperfusion in rats and to explore the protective effect of LMWH on neurons after ischemia / reperfusion And possible mechanism. Methods The middle cerebral artery occlusion model (MCAO) was established by Zea Longa method. One hundred and forty SD rats were randomly divided into sham operation group, ischemia reperfusion group (MCAO group) and LMWH intervention group. Each group of rats were randomly divided into 4 groups: 6h, 24h, 48h, 96h after reperfusion respectively. TUNEL staining was used to detect apoptosis in the ischemic area and NR1 mRNA was detected by in situ hybridization. Results The expression of apoptotic cells and NR1 mRNA in infarcted cerebral cortex of MCAO group was significantly increased compared with that of sham-operation group (P <0.01). However, LMWH-treated group failed to prevent apoptosis after reperfusion and the number of positive cells was 48h (P <0.01), but compared with MCAO group, the number of apoptotic cells decreased significantly (P <0.01). Conclusion The expression of NR1 mRNA in brain tissue after reperfusion is increased, which is closely related to apoptosis. Low molecular weight heparin may inhibit the apoptosis of ischemic penumbra by inhibiting the expression of NR1 mRNA.