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

• Published in: Life sciences (1973) Vol. 279; p. 119660
• Main Authors: Dong, Ling-di, Ma, Yan-mei, Xu, Jie, Guo, Yong-zhen, Yang, Lan, Guo, Feng-Ying, Wang, Min-Xing, Jing, Li, Zhang, Jian-Zhong
• Format: Journal Article
• Language: English
• Published: New York Elsevier Inc 15.08.2021; Elsevier BV
• Subjects: Apoptosis; astrocytes; Brain damage; Brain injury; CD11b antigen; CD16 antigen; CD86 antigen; Cerebral blood flow; Cerebral ischemia-reperfusion; Diabetes; Diabetes mellitus; Hyperglycemia; infarction; Inflammation; Injuries; Ischemia; Microglia; Neurological diseases; Occlusion; Polarization; Reperfusion; Polarization; Hyperglycemia; Cerebral ischemia-reperfusion; Microglia
• ISSN: 0024-3205; 1879-0631; 1879-0631
• DOI: 10.1016/j.lfs.2021.119660

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.