【摘要】：目的 探究大黃酚(Chrysophanol,CHR)對大腦中動脈梗死(middle cerebral artery occlusion,MCAO)模型小鼠再灌注后腦內(nèi)環(huán)氧化酶2(cyclooxygenase-2,COX2)和基質(zhì)金屬蛋白酶-9(matrix metalloproteinase-9,MMP-9)表達的影響,探討CHR保護腦缺血再灌注損傷的抗炎機制。方法 采用數(shù)字表法隨機將18只健康雄性C57BL小鼠分為3組:假手術(Sham)組、MCAO組、CHR組(小鼠造模當天按0.1 mg/kg腹腔注射CHR,此后每天1次,連續(xù)給藥14 d),每組6只。使用線栓法制作小鼠右側(cè)大腦中動脈缺血45 min再灌注模型。術中監(jiān)測小鼠肛溫,使其維持在正常范圍。于再灌注后14 d處死小鼠,迅速取腦,用免疫熒光染色檢測小鼠腦組織冰凍切片缺血半暗帶區(qū)COX2和MMP-9的表達,并用免疫熒光雙標法對COX2和MMP-9在缺血腦組織的表達進行細胞定位。結(jié)果 1)Sham組小鼠偶見COX2或MMP-9染色陽性細胞。與Sham組相比,MCAO組小鼠腦缺血半暗帶區(qū)COX2和MMP-9的表達明顯增高(P0.05)。2)與MCAO組相比,給予CHR治療后,缺血再灌注小鼠腦缺血半暗帶區(qū)COX2和MMP-9的表達均明顯減少(P0.05)。3)缺血再灌注小鼠腦缺血半暗帶區(qū),COX2或MMP-9免疫熒光染色分別與神經(jīng)元標志物Neu N免疫熒光染色共定位。結(jié)論 CHR可能通過抑制COX2和MMP-9的蛋白表達,減輕炎性反應,從而對腦缺血再灌注損傷發(fā)揮長期的神經(jīng)保護作用。
[Abstract]:Objective to investigate the effects of chrysophanol (Chrysophanol,CHR) on the expression of cyclooxygenase-2 (cyclooxygenase-2,COX2) and matrix metalloproteinase-9 (matrix metalloproteinase-9,MMP-9) after reperfusion in (middle cerebral artery occlusion,MCAO model mice with middle cerebral artery infarction. To investigate the anti-inflammatory mechanism of CHR in the protection of cerebral ischemia reperfusion injury. Methods 18 healthy male C57BL mice were randomly divided into 3 groups: sham operation (Sham) group, MCAO group and CHR group (mice were injected with CHR, once a day according to 0.1 mg/kg per day after CHR, was injected intraperitoneally for 14 d),). There were 6 rats in each group. The right middle cerebral artery (MCAA) ischemia reperfusion model of mice was established with thread occlusion for 45 min. The anus temperature of mice was monitored during operation to keep it in normal range. The mice were killed 14 days after reperfusion. The expression of COX2 and MMP-9 in the ischemic penumbra of frozen sections of the brain were detected by immunofluorescence staining. The expression of COX2 and MMP-9 in ischemic brain tissue was detected by immunofluorescence double labeling method. Results 1) COX2 or MMP-9 positive cells were occasionally found in Sham group mice. Compared with Sham group, the expression of COX2 and MMP-9 in cerebral ischemic penumbra in MCAO group was significantly higher than that in Sham group (P0.05). Compared with MCAO group, the expression of COX2 and MMP-9 in MCAO group was significantly higher than that in MCAO group. The expression of COX2 and MMP-9 in cerebral ischemic penumbra decreased significantly in ischemia-reperfusion mice (P0.05). COX2 or MMP-9 immunofluorescence staining were co-located with Neu N immunofluorescence staining. Conclusion CHR may play a long-term neuroprotective role in cerebral ischemia-reperfusion injury by inhibiting the expression of COX2 and MMP-9 proteins and reducing inflammatory response.
【作者單位】： 首都醫(yī)科大學宣武醫(yī)院北京市老年病醫(yī)療研究中心神經(jīng)變性病教育部重點實驗室腦血管病轉(zhuǎn)化醫(yī)學北京市重點實驗室;
【分類號】：R743.3

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