CAJ | 학술논문

目的：探讨米诺环素对大鼠嗜铬细胞瘤细胞（PC12）缺氧缺糖（OGD）损伤后细胞存活率及神经突生长的影响。方法分别缺氧缺糖2、4、6h及8h建立PC12细胞OGD损伤模型，将细胞分为正常对照组，OGD组和不同浓度的（0．1、1．0μM和10．0μM）米诺环素治疗组，在缺氧缺糖／复氧24h后，用CCK‐8法检测细胞存活率，免疫荧光法标记MAP‐2并在荧光显微镜下观察神经突的生长，Westernblot法检测各组GAP‐43蛋白的表达水平。结果与OGD组比较，米诺环素能显著提OGD后PC12细胞的存活率［（46．1±2．9）％vs．（77．0±2．5）％，P＜0．01］，促进PC12细胞OGD损伤后神经突的生长，同时上调轴突再生蛋白GAP‐43的表达［（0．34±0．04）vs．（2．11±0．10），P＜0．01］。结论米诺环素能减轻OGD损伤所致PC12细胞的死亡，并促进细胞神经突的生长。
목적：탐토미낙배소대대서기락세포류세포（PC12）결양결당（OGD）손상후세포존활솔급신경돌생장적영향。방법분별결양결당2、4、6h급8h건립PC12세포OGD손상모형，장세포분위정상대조조，OGD조화불동농도적（0．1、1．0μM화10．0μM）미낙배소치료조，재결양결당／복양24h후，용CCK‐8법검측세포존활솔，면역형광법표기MAP‐2병재형광현미경하관찰신경돌적생장，Westernblot법검측각조GAP‐43단백적표체수평。결과여OGD조비교，미낙배소능현저제OGD후PC12세포적존활솔［（46．1±2．9）％vs．（77．0±2．5）％，P＜0．01］，촉진PC12세포OGD손상후신경돌적생장，동시상조축돌재생단백GAP‐43적표체［（0．34±0．04）vs．（2．11±0．10），P＜0．01］。결론미낙배소능감경OGD손상소치PC12세포적사망，병촉진세포신경돌적생장。
Objective To investigate the effects of minocycline on cell viability and neurite outgrowth of pheochromocytoma cells (PC12) after oxygen‐glucose deprivation(OGD) injury .Methods PC12 cells were exposed to OGD insult for 2 ,4 ,6 ,8 h to estab‐lish a cerebral ischemia model in vitro .High‐differentiated PC12 cells were cultivated and randomly divided into three groups :con‐trol group ,OGD group and various doses of minocycline(0 .1 ,1 .0 ,10 .0 μM) treated group .24 h after OGD‐reperfusion ,PC12 cells viability was assessed by CCK‐8 assay ,the neurite was labeled with MAP‐2 by immunofluorescence and neurite length was meas‐ured by the Image‐Pro Plus 7 .0 software ,GAP‐43 protein expression was determined by Western blotting .Results Compared to the OGD groups ,minocycline induced a concentration‐dependent increase in cells viability [(46 .1 ± 2 .9)% vs .(77 .0 ± 2 .5)% ,P<0.01],improvedneuriteoutgrowthandincreasedtheexpressionofGAP‐43proteininPC12cellsafterOGDinjury([(0.34±0.04) vs .(2 .11 ± 0 .10) ,P<0 .01] .Conclusion Minocycline could protect against oxygen glucose deprivation injury and promote neurite outgrowth .This finding suggests minocycline may be a novel therapy for cerebral ischemia .