CAJ | 학술논문

目的：探讨米诺环素（ MC）的脑缺血保护作用及可能机制。方法健康雄性SD大鼠（250±30） g随机分成假手术组、缺血再灌注组、MC低剂量干预组、MC高剂量干预组，建立大鼠右侧大脑中动脉阻断（ middle cerebral artery occulusion ，MCAO）局灶性脑缺血再灌注模型，按再灌注不同时点（2、6、12、24和48 h）随机分为5个亚组，每组6只，用于神经功能缺损评分、脑梗死面积测定及反转录聚合酶链反应法（ RT-PCR）半定量检测mGluR1-mRNA的表达水平。结果造模术后，缺血再灌注组及MC干预组均出现一定程度神经功能障碍，与缺血再灌注组相比，MC干预组神经功能评分降低，脑梗死面积减少，mGluR1-mRNA的表达降低，差异有统计学意义（P＜0．05）。结论米诺环素可降低缺血再灌注大鼠的神经功能评分，缩小缺血再灌注大鼠的脑梗死面积，减少mGluR1-mRNA表达。这可能是米诺环素神经保护作用的机制之一。
목적：탐토미낙배소（ MC）적뇌결혈보호작용급가능궤제。방법건강웅성SD대서（250±30） g수궤분성가수술조、결혈재관주조、MC저제량간예조、MC고제량간예조，건립대서우측대뇌중동맥조단（ middle cerebral artery occulusion ，MCAO）국조성뇌결혈재관주모형，안재관주불동시점（2、6、12、24화48 h）수궤분위5개아조，매조6지，용우신경공능결손평분、뇌경사면적측정급반전록취합매련반응법（ RT-PCR）반정량검측mGluR1-mRNA적표체수평。결과조모술후，결혈재관주조급MC간예조균출현일정정도신경공능장애，여결혈재관주조상비，MC간예조신경공능평분강저，뇌경사면적감소，mGluR1-mRNA적표체강저，차이유통계학의의（P＜0．05）。결론미낙배소가강저결혈재관주대서적신경공능평분，축소결혈재관주대서적뇌경사면적，감소mGluR1-mRNA표체。저가능시미낙배소신경보호작용적궤제지일。
Objective To explore the neuroprotective effect and mechanism of minocycline on focal cerebral ischemia /reperfusion . Methods Healthy male SD rats ( 250 ±30 ) g were randomized into sham group , ischemia/reperfusion group , minocycline low dose group,minocycline high dose group ,for establishing the acute focal cerebral ischemia/reperfusion models with 30 rats in each group. According to different reperfusion time (2,6,12,24 and 48 h),each group was randomized into five subgroups (each group n=6), which were used for nerve function defect evaluation ,cerebral infarction area measurement and detection of mGluR 1-mRNA expression level by reverse transcription polymerase chain reaction method ( RT-PCR) .Results The ischemia reperfusion group and MC interven-tion group both had nerve dysfunction to a certain degree .Neural function score ,cerebral infarction area and mGluR 1-mRNA expression were reduced in the MC intervention group compared with those in the ischemia reperfusion group (P<0.05).Conclusions Minocy-cline can reduce neurologic severity scores , cerebral infarction volume and mGluR 1-mRNA expressions in ischemia-reperfusion rats , which may be one of the neuroprotective mechanism of minocycline .