神经损伤与功能重建
神經損傷與功能重建
신경손상여공능중건
NEURAL INJURY AND FUNCTIONAL RECONSTRUCTION
2014年
5期
369-372
,共4页
张秋佳%杨锦珊%刘阳%王伟
張鞦佳%楊錦珊%劉暘%王偉
장추가%양금산%류양%왕위
MRS2179%缺血性脑卒中%血脑屏障%脑水肿%基质金属蛋白酶-9
MRS2179%缺血性腦卒中%血腦屏障%腦水腫%基質金屬蛋白酶-9
MRS2179%결혈성뇌졸중%혈뇌병장%뇌수종%기질금속단백매-9
MRS2179%ischemic cerebral stroke%blood-brain barrier%brain edema%matrix metalloproteinase-9
目的：观察P2Y1受体抑制剂MRS2179对大鼠缺血性脑卒中后MMP-9表达及血脑屏障（BBB）通透性的影响。方法：45只SD大鼠随机分成假手术组、模型组、MRS2179组各15只。假手术组及模型组经侧脑室注射5滋L人工脑脊液（aCSF），MRS2179组侧脑室注射5滋L MRS2179（2 nmol）。制备大脑中动脉阻塞（MCAO）模型，假手术组不予缺血。缺血再灌注24 h后，应用干湿重法检测脑组织含水量；伊文思蓝染料（EB）溢出量定量检测BBB通透性改变；Western blot法检测MMP-9蛋白表达。结果：模型组、假手术组、MRS2179组的脑含水量分别为（81.72依0.23）%、（77.65依0.27）%、（79.92依0.24）%（n=6），模型组高于假手术组（<0.01）；MRS2179组较模型组有所下降（<0.01），但仍高于假手术组（<0.01）。模型组梗死侧脑组织血管外EB溢出量为（1737.60依67.46）ng/g，显著高于假手术组（324.18依63.35）ng/g（<0.01）；MRS2179组梗死侧脑组织血管外EB溢出量为（1165.15依93.26）ng/g，较模型组明显下降（<0.01）（n=6）。假手术组、模型组、MRS2179再灌注24 h梗死边缘区脑组织中相对MMP-9蛋白含量分别为（0.52依0.05）、（1.69依0.08）、（0.99依0.10）（n=3），模型组与假手术组相比明显升高（<0.01），MRS2179组与模型组比较显著下降（<0.01）。结论：P2Y1R抑制剂MRS2179可能通过降低MMP-9表达，降低BBB通透性，减轻缺血性脑卒中后脑水肿程度。
目的：觀察P2Y1受體抑製劑MRS2179對大鼠缺血性腦卒中後MMP-9錶達及血腦屏障（BBB）通透性的影響。方法：45隻SD大鼠隨機分成假手術組、模型組、MRS2179組各15隻。假手術組及模型組經側腦室註射5滋L人工腦脊液（aCSF），MRS2179組側腦室註射5滋L MRS2179（2 nmol）。製備大腦中動脈阻塞（MCAO）模型，假手術組不予缺血。缺血再灌註24 h後，應用榦濕重法檢測腦組織含水量；伊文思藍染料（EB）溢齣量定量檢測BBB通透性改變；Western blot法檢測MMP-9蛋白錶達。結果：模型組、假手術組、MRS2179組的腦含水量分彆為（81.72依0.23）%、（77.65依0.27）%、（79.92依0.24）%（n=6），模型組高于假手術組（<0.01）；MRS2179組較模型組有所下降（<0.01），但仍高于假手術組（<0.01）。模型組梗死側腦組織血管外EB溢齣量為（1737.60依67.46）ng/g，顯著高于假手術組（324.18依63.35）ng/g（<0.01）；MRS2179組梗死側腦組織血管外EB溢齣量為（1165.15依93.26）ng/g，較模型組明顯下降（<0.01）（n=6）。假手術組、模型組、MRS2179再灌註24 h梗死邊緣區腦組織中相對MMP-9蛋白含量分彆為（0.52依0.05）、（1.69依0.08）、（0.99依0.10）（n=3），模型組與假手術組相比明顯升高（<0.01），MRS2179組與模型組比較顯著下降（<0.01）。結論：P2Y1R抑製劑MRS2179可能通過降低MMP-9錶達，降低BBB通透性，減輕缺血性腦卒中後腦水腫程度。
목적：관찰P2Y1수체억제제MRS2179대대서결혈성뇌졸중후MMP-9표체급혈뇌병장（BBB）통투성적영향。방법：45지SD대서수궤분성가수술조、모형조、MRS2179조각15지。가수술조급모형조경측뇌실주사5자L인공뇌척액（aCSF），MRS2179조측뇌실주사5자L MRS2179（2 nmol）。제비대뇌중동맥조새（MCAO）모형，가수술조불여결혈。결혈재관주24 h후，응용간습중법검측뇌조직함수량；이문사람염료（EB）일출량정량검측BBB통투성개변；Western blot법검측MMP-9단백표체。결과：모형조、가수술조、MRS2179조적뇌함수량분별위（81.72의0.23）%、（77.65의0.27）%、（79.92의0.24）%（n=6），모형조고우가수술조（<0.01）；MRS2179조교모형조유소하강（<0.01），단잉고우가수술조（<0.01）。모형조경사측뇌조직혈관외EB일출량위（1737.60의67.46）ng/g，현저고우가수술조（324.18의63.35）ng/g（<0.01）；MRS2179조경사측뇌조직혈관외EB일출량위（1165.15의93.26）ng/g，교모형조명현하강（<0.01）（n=6）。가수술조、모형조、MRS2179재관주24 h경사변연구뇌조직중상대MMP-9단백함량분별위（0.52의0.05）、（1.69의0.08）、（0.99의0.10）（n=3），모형조여가수술조상비명현승고（<0.01），MRS2179조여모형조비교현저하강（<0.01）。결론：P2Y1R억제제MRS2179가능통과강저MMP-9표체，강저BBB통투성，감경결혈성뇌졸중후뇌수종정도。
Objective:To observe the effects of selective P2Y1R antagonist, MRS2179, on the expression of MMP-9 and the blood-brain barrier (BBB) permeability in a rat model of middle cerebral artery occlusion(MCAO). Methods:All 45 SD rats were randomized into 3 groups:sham group (n=15), model group (n=15)and MRS2179 group (n=15). Intracerebroventricular administration of 5 μL vehicle control (aCSF) was performed to the sham group and the model group. Meanwhile, 5μL of MRS2179 (2 nmol) was given to the rats in the MRS2179 group in the same way. The MCAO models were made in the groups control and MRS2179.The sham group was treated in the same manner as those undergoing MCAO, however, no occluding thread was inserted. After 24 h reperfu-sion, the wet/dry method was used to evaluate the brain water content of the ischemic hemisphere, the Evans Blue dye (EB) extravasation was measured to assess the BBB permeability and the expression of MMP-9 was deter-mined by Western blot. Results:The brain water content in the model group, the sham group and the MRS2179 group was (81.72±0.23)%, (77.65±0.27)%, (79.92±0.24)%respectively(n=6). Compared with the model group, the brain water content in the MRS2179 group was decreased, but was still higher than that in the sham group ( <0.01) .The EB extravasation from the ischemic hemisphere in the model group was (1737.60±67.46)ng/g, remarkably higher than those in the in the MRS2179 group [(1165.15±93.26)ng/g] and sham group [(324.18±63.35)ng/g] ( <0.01) (n=6). In terms of the expression of MMP-9 in the ischemic penumbra, the protein amount was (0.52±0.05), (1.69±0.08) and (0.99±0.10) respectively in the sham group, the model group and the MRS2179 group (n=3). The protein amount in the MRS2179 group was significantly lower than that in the model group ( <0.01). Conclusion:Inhibition of P2Y1R by MRS2179 might reduce the BBB permeability and relieve brain edema after the ischemic cerebral stroke by decreasing the expression of MMP-9.
