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脑缺血再灌注损伤后高血糖对大鼠小胶质细胞极化的影响。

Effect of hyperglycemia on microglial polarization after cerebral ischemia-reperfusion injury in rats.

机构信息

Department of Pathology, School of Basic Medical Science, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia 750004, China; Department of Dermatology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, China.

Department of Pathology, School of Basic Medical Science, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia 750004, China.

出版信息

Life Sci. 2021 Aug 15;279:119660. doi: 10.1016/j.lfs.2021.119660. Epub 2021 May 27.

Abstract

Hyperglycemia has been shown to aggravate ischemic brain damage, in which the inflammatory reaction induced by hyperglycemia is involved in the worsening of cerebral ischemia-reperfusion injury. However, the role of microglial polarization in hyperglycemia-aggravating cerebral ischemia-reperfusion injury remains unknown. The present study investigated whether diabetic hyperglycemia inhibited or activated microglia, as well as microglial subtypes 1 and 2. Rats were used to establish the diabetic hyperglycemia and middle cerebral artery occlusion (MCAO) model. The markers CD11b, CD16, CD32, CD86, CD206, and Arg1 were used to show M1 or M2 microglia. The results revealed increased neurological deficits, infarct volume, and neural apoptosis in rats with hyperglycemia subjected to MCAO for 30 min and reperfused at 1, 3, and 7 days compared with the normoglycemic rats. Microglia and astrocyte activation and proliferation were inhibited in hyperglycemic rats. Furthermore, M1 microglia polarization was promoted, while that of M2 microglia was inhibited in hyperglycemic rats. These findings suggested that the polarization of M1 and M2 microglia is activated and inhibited, respectively, in hyperglycemic rats and may be involved in the aggravated brain damage caused by ischemia-reperfusion in diabetic hyperglycemia.

摘要

高血糖已被证明会加重缺血性脑损伤,其中高血糖诱导的炎症反应参与了脑缺血再灌注损伤的恶化。然而,小胶质细胞极化在高血糖加重脑缺血再灌注损伤中的作用尚不清楚。本研究旨在探讨糖尿病高血糖是否抑制或激活了小胶质细胞,以及小胶质细胞 1 型和 2 型。使用大鼠建立糖尿病高血糖和大脑中动脉闭塞(MCAO)模型。使用 CD11b、CD16、CD32、CD86、CD206 和 Arg1 标志物来显示 M1 或 M2 小胶质细胞。结果显示,与正常血糖组大鼠相比,高血糖组大鼠在 MCAO 30 分钟后再灌注 1、3 和 7 天时,神经功能缺损、梗死体积和神经细胞凋亡增加。高血糖大鼠的小胶质细胞和星形胶质细胞激活和增殖受到抑制。此外,高血糖大鼠的 M1 小胶质细胞极化被促进,而 M2 小胶质细胞极化被抑制。这些发现表明,在高血糖大鼠中,M1 和 M2 小胶质细胞的极化分别被激活和抑制,这可能与糖尿病高血糖引起的缺血再灌注加重的脑损伤有关。

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