高脂血症大鼠脑缺血/再灌注后p38 MAPK活化及对Bax和Bcl-2表达的影响

doi:10.16098/j.issn.0529-1356.2023.01.007

摘要/Abstract

摘要：

目的检测高脂血症大鼠脑缺血/再灌注（I/R）损伤后大脑皮质内磷酸化p38 MAPK （p-p38 MAPK）、Bax和Bcl-2表达变化，及SB203580对p-p38 MAPK、Bax和Bcl-2表达的影响，研究在高脂血症脑I/R损伤中 p38 MAPK 活化对Bax和Bcl-2表达的影响。方法大鼠高脂血症模型建立后，将其随机分为3组，假手术组（sham）、手术组（I/R）、SB203580处理组（SB+I/R），每组10只。线栓法建立左侧大脑中动脉栓塞I/R模型，神经行为学评分观察大鼠神经行为损伤症状，2,3,5-氯化三苯基四氮唑（TTC）染色显示脑梗死灶，TUNEL染色观察凋亡细胞，免疫组织化学法分析p-p38 MAPK、Bax和Bcl-2相对表达水平。结果与sham组比较，I/R组大鼠脑梗死体积百分比、细胞凋亡指数和神经行为学评分均显著升高，且p-p38 MAPK、Bax表达明显增高，Bcl-2表达明显降低，差异均具有统计学意义(P<0.05)。与I/R组比较，SB+I/R组大鼠脑组织损伤减轻，梗死灶明显缩小，细胞凋亡指数明显降低，p-p38 MAPK表达明显降低，Bax表达减少而Bcl-2表达增多，差异均有统计学意义(P<0.05)。SB+I/R组较I/R组神经行为学评分降低，但差异无统计学意义。结论在高脂血症大鼠脑缺血再灌注损伤过程中，p38 MAPK活化可调节Bax和Bcl-2的表达。

关键词: 高脂血症, 脑缺血/再灌注损伤, 磷酸化p38丝裂原活化蛋白激酶, Bcl-2相关X蛋白, B淋巴细胞瘤-2, SB203580, 免疫组织化学, 大鼠

Abstract:

Objective To detecte the expressions of phosphorylated p38 MAPK (p-p38 MAPK), Bax and Bcl-2 in the cerebral cortex of hyperlipidemia rats after cerebral ischemia-reperfusion (I/R) injury and the effect of SB203580 on the expressions of p-p38 MAPK, Bax and Bcl-2, to explore the effect of p38 MAPK activation on the expressions of Bax and Bcl-2 in hyperlipidemia cerebral I/R injury. Methods After the hyperlipidemia model was established, the rats were randomly divided into 3 groups: sham operation group, operation group (I/R) and SB203580 treatment group (SB+I/R), with 10 rats in each group. The focal cerebral I/R model in hyperlipemia rats was established with thread embolism of the left middle cerebral artery. The neurobehavioral score was used to observe the symptoms of neurobehavioral injury. The 2,3,5-triphenyltetrazolium chloride (TTC) staining was used to detect the volume of cerebral infarction, and the TUNEL staining was used to observe apoptotic cells. The relative expression levels of p-p38 MAPK, Bax and Bcl-2 were analyzed by immunohistochemistry. Results Compared with the sham group, the infarct volume, apoptosis index and neurobehavioral score of rats in the I/R group increased significantly, and the expressions of p-p38 MAPK and Bax increased significantly, and the expression of Bcl-2 decreased significantly (P<0.05). Compared with the I/R group, rats in the SB+I/R group had less brain damage, the infarct volume and the apoptosis index were significantly reduced, the expressions of p-p38 MAPK reduced significantly, Bax expression decreased while Bcl-2 expression increased. The differences were statistically significant (P<0.05). Neurobehavioral scores were lower in SB+I/R group than in I/R group, but the difference was not statistically significant. Conclusion In the process of cerebral I/R injury in hyperlipidemiarats, activation of p38 MAPK can regulate the expression of Bax and Bcl-2.

Key words: Hyperlipidemia, Cerebral ischemia-reperfusion, Phosphorylated-p38 mitogen activated protein kinase, Bcl-2 assaciated X protein, B-cell lymphoma-2, SB203580, Immunohistochemistry, Rat

中图分类号:

R322.8

高赛红张小良杨迎春乔海兵. 高脂血症大鼠脑缺血/再灌注后p38 MAPK活化及对Bax和Bcl-2表达的影响[J]. 解剖学报, 2023, 54(1): 50-55.

GAO Sai-hong ZHANG Xiao-liang YANG Ying-chun QIAO Hai-bing. Activation of p38 MAPK and its effect on the expression of Bax and Bcl-2 after cerebral ischemia-reperfusion in hyperlipidemia rats[J]. Acta Anatomica Sinica, 2023, 54(1): 50-55.

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