摘要
目的 探讨钙离子通道在缺氧缺糖/再灌注诱导皮质神经元损伤中的作用.方法 采用培养的大鼠皮质神经元缺氧缺糖模型,应用DAPI染色方法,以细胞凋亡率为指标,观察缺氧缺糖诱导神经兀损伤及Ca2＋螯合剂EGTA、NMDA受体拮抗剂MK-801、L-型电压门控钙通道（L-VGCC）拮抗剂尼莫地平、蛋白酪氨酸激酶（PTK）抑制剂染料木黄酮、CaMKⅡ抑制剂NK-62对缺氧缺糖/再灌注诱导神经元损伤的作用.结果 缺氧缺糖/再灌注诱导细胞发生凋亡,至再灌注24 h凋亡率达到80%左右;加入EGTA、MK-801及尼莫地平可以抑制细胞凋亡,凋亡率从80%分别降低为33%、35%和38%;加入染料木黄酮和KN-62可以使凋亡率从80%分别降低为43%和42%.结论 减少胞外Ca2＋浓度、阻断NMDA受体和L-VGCC、抑制蛋白酪氨酸激酶和CaMKⅡ可以减少缺氧缺糖/再灌注诱导的神经元损伤.缺氧缺糖/再灌注诱导的神经元损伤可能与胞外ca2＋内流有关,并与NMDA受体和L-VGCC两类钙通道的开放有关.
Objective To study the roles of calcium channels in cultured cortical neuronal injury induced by oxygen -glucose deprivation （OGD）. Methods We investigated the apoptosis of cultured cortical neurons induced by OGD and reoxygen. We also evaluated the effects of EGTA （the eliminator of extracellular Ca^2＋ ） , MK -801 （a selective antagonist of NMDA receptor）, nimodipine （ the blocker of L - type voltage - gated calcium channel, L - VGCC ）, genistein （ the inhibitor of PTK） and KN - 62 （ the inhibitor of CaMK II ） on the delayed neuronal death in cultured cortical neurons. Results The apoptosis of cultured cortical neurons was induced by OGD and reoxygen. Then the apoptotic rates peaked at 80% at 24 h of reoxygen. The apoptotic rates were decreased by EGTA, MK - 801 and nimodipine from 80% to 33% , 35% and 38% , respectively. While genistein and KN - 62 decreased the proportion of apoptotic cells from 80% to 43% and 42%. Conclusion The eliminator of extracellular Ca^2＋, the blocker of NMDA receptor and L - VGCC, the inhibitor of PTK and CaMK II may decrease the apoptosis - like cell death induced by OGD. These results suggest that apoptosis of cortical neurons induced by OGD and reoxygen may be associated with the extracelluar Ca^2＋ influx and the openness of NMDA receptor and L - VGCC.
出处
《徐州医学院学报》
CAS
2011年第12期783-787,共5页
Acta Academiae Medicinae Xuzhou
基金
基金项目：国家自然科学基金面上项目（30170220）
徐州市科技计划项目（XZZDll57）
徐州医学院院长基金（2011KJZ03）
关键词
缺氧缺糖
神经元损伤
NMDA受体
L-型电压门控钙通道
oxygen - glucose deprivation
neuronal injury
NMDA receptor
L - type voltage - gated calcium channel
