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目的分析活化小胶质细胞(MG)在急性脑梗死中的作用机制。方法选择30只清洁级成年雄性昆明小鼠,随机均分为3组,每组10只,即空白对照组、安慰剂组、小胶质细胞移植组,建立急性脑梗死模型,空白对照组不予任何处理,小胶质细胞移植组术后12h注入50μL MG悬液,安慰剂组术后12h注入剂量相同培养基,测定脑梗死体积,测定细胞凋亡指数,测定各组细胞外信号调激酶1/2(ERK1/2)蛋白及脑源性神经营养因子(BDNF)阳性表达情况。结果 (1)安慰剂组脑梗死面积明显高于小胶质细胞移植组(P<0.05);(2)安慰剂组凋亡细胞阳性率高于小胶质细胞移植组(P<0.05);(3)移植12h,各组p ERK1/2阳性率对比差异无统计学意义(P>0.05),移植24h、72h,空白对照组、安慰剂组p ERK1/2阳性率无明显变化(P>0.05),小胶质细胞移植组p ERK1/2阳性率明显上升,高于其他两组(P<0.05);(4)空白对照组、安慰剂组BDNF阳性细胞所占比例对比差异无统计学意义(P>0.05),小胶质细胞移植组BDNF阳性率均高于空白对照组与安慰剂组,对比差异有统计学意义(P<0.05)。结论活化MG在急性脑梗死中有其神经保护机制,可促进神经细胞内ERK1/2磷酸化,增加BDNF合成,减少细胞凋亡。
Objective To analyze the mechanism of activated microglial cells (MG) in acute cerebral infarction. Methods Thirty male Kunming mice of clean grade were randomly divided into three groups (n = 10), namely blank control group, placebo group and microglial transplantation group. The acute cerebral infarction model was established. The blank control group In any group, 50 microg MG suspension was injected into the microglial transplantation group 12h after operation, and the same medium was injected into the placebo group 12h after operation. The infarct volume was measured and the apoptosis index was measured. The extracellular signal-regulated kinase 1/2 (ERK1 / 2) protein and brain-derived neurotrophic factor (BDNF) positive expression. Results (1) The area of cerebral infarction in placebo group was significantly higher than that in microglial transplantation group (P <0.05). (2) The positive rate of apoptotic cells in placebo group was higher than that of microglial transplantation group (P <0.05). There was no significant difference in the positive rate of p ERK1 / 2 between the two groups (P> 0.05). The positive rates of p ERK1 / 2 in blank control group and placebo group had no significant change at 24h and 72h after transplantation (P> 0.05). The positive rate of p ERK1 / 2 in microglial transplantation group was significantly higher than that in other two groups (P <0.05). (4) There was no significant difference in the proportion of BDNF positive cells between blank control group and placebo group (P> 0.05). The positive rate of BDNF in microglial transplantation group was higher than that in blank control group and placebo group, the difference was statistically significant (P <0.05). Conclusion Activated MG has neuroprotective mechanism in acute cerebral infarction, which can promote the phosphorylation of ERK1 / 2 in nerve cells, increase the synthesis of BDNF and decrease the apoptosis rate.