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目的观察脑缺血再灌注(I/R)损伤大鼠脑组织中补体C1q与C3c的表达,探讨补体反应与小胶质细胞在脑I/R损伤中的作用及其机制。方法 48只SD雄性大鼠随机分为正常对照组、假手术组、I/R模型24 h、72 h、7 d、15 d组,线栓法建立局灶性大脑中动脉闭塞再灌注模型。尼氏体染色观察神经元结构,免疫组化法检测CD11b以及C1q、C3c的表达水平。结果与sham组相比,I/R 24 h组脑组织尼氏体染色加深,随后染色反应减弱,尤以I/R 72 h组减少最为显著;I/R 24 h组脑组织CD11b表达增多且在I/R 72 h组达到峰值,随后逐渐减少,与sham组比较,全部模型组差异显著(P<0.05);I/R 24 h组脑组织C1q与C3c急剧增多且在I/R 7 d组达到峰值,随后见下降趋势,全部模型组与sham组比较差异显著(P<0.05)。结论脑I/R损伤大鼠脑组织中C1q、C3c与CD11b的表达呈正相关。提示脑I/R损伤后,启动了脑内固有免疫反应,补体C1q与C3c活化,同时激活小胶质细胞,在脑I/R损伤中起到保护或损伤作用。
Objective To investigate the expression of complement C1q and C3c in the brain tissue of rats with cerebral ischemia-reperfusion (I / R) injury and to explore the role of complement reaction and microglia in brain I / R injury. Methods 48 SD male rats were randomly divided into normal control group, sham operation group, I / R model 24 h, 72 h, 7 d and 15 d groups. The focal middle cerebral artery occlusion and reperfusion model was established by thread occlusion. Nissl staining was used to observe the neuronal structure. The expression of CD11b, C1q and C3c were detected by immunohistochemistry. Results Compared with the sham group, the Nissl staining in brain tissue of I / R 24 h group was deepened, and then the staining reaction was weakened, especially in I / R 72 h group. The expression of CD11b in I / R 24 h group was increased (P <0.05). Compared with Sham group, the levels of C1q and C3c in I / R group increased sharply at I / R 7 h and decreased significantly at I / R 7 d Group reached the peak, then see the downward trend, all the model group and sham group difference was significant (P <0.05). Conclusion The expressions of C1q, C3c and CD11b in the brain of rats with brain I / R injury are positively correlated. Prompted brain I / R injury, the brain initiated an innate immune response, complement C1q and C3c activation, while activating microglia, play a protective or damaging role in brain I / R injury.