miR-155通过调控Th9细胞分化及相关因子表达参与脑梗死免疫发病机制的研究-东南大学学报医学版

miR-155通过调控Th9细胞分化及相关因子表达参与脑梗死免疫发病机制的研究

单位：鄂州市中心医院神经内科, 湖北鄂州 436000

分类号：R743.33

出版年·卷·期（页码）：2022·41·第三期（408-414）

摘要：

目的：探究微小RNA（microRNA，miR）-155参与脑梗死的免疫发病机制。方法：通过栓线法构建脑梗死大鼠模型。将30只脑梗死大鼠随机均分为脑梗死组和脑梗死+miR-155抑制剂组。另取15只假手术大鼠作为对照组。检测各组神经功能（mNSS评分）、梗死体积、神经元凋亡、炎症细胞因子水平，分析脑组织血液中Th9细胞比例和白细胞介素（IL）-9的水平，以及T淋巴细胞中miR-155、转录因子PU.1和IRF4蛋白的表达水平。结果：脑梗死组mNSS评分、梗死体积、凋亡指数、IL-1β水平、IL-6水平、Th9细胞比例、IL-9水平、miR-155以及PU.1、IRF4蛋白的表达水平均显著高于对照组（均P<0.05）。脑梗死+miR-155抑制剂组mNSS评分、梗死体积、凋亡指数、IL-1β水平、IL-6水平、Th9细胞比例、IL-9水平、miR-155以及PU.1、IRF4蛋白的表达水平均显著低于脑梗死组（均P<0.05），但均显著高于对照组（均P<0.05）。结论：miR-155可能通过提高Th9细胞比例和IL-9的表达促进免疫炎症反应，从而导致神经元损伤参与脑梗死进展。

Objective: To explore the effects of microRNA(miR)-155 in the immune pathogenesis of cerebral infarction animal models. Methods: The rat model of cerebral infarction was constructed by the thread embolism method. Thirty rats with cerebral infarction were randomly divided into cerebral infarction group(n=15) and cerebral infarction+miR-155 inhibitor group(n=15). Fifteen sham-operated rats served as the control group. Nerve function, infarct volume, neuronal apoptosis, inflammatory cytokine levels in each group were detected, so were the proportion of Th9 cells and IL-19 levels in brain tissue, miR-155, protein expressions of PU.1 and IRF4 in T lymphocytes. Results: The mNSS score, infarct volume, apoptosis index, IL-1β, IL-6, Th9 cell ratio, IL-9 level, miR-155 and PU.1 and IRF4 protein expression levels in the cerebral infarction group were significantly higher than those in the control group(P<0.05). The mNSS score, infarct volume, apoptosis index, IL-1β, IL-6, Th9 cell ratio, IL-9 level, miR-155 and PU.1 and IRF4 protein expression levels in the cerebral infarction+miR-155 inhibitor group were significantly lower than those in the cerebral infarction group(P<0.05), and were significantly higher than those in control group(P<0.05). Conclusion: miR-155 may promote immune inflammatory response by increasing the proportion of Th9 and the expression of IL-9, leading to neuronal damage and participating in the progression of cerebral infarction.

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