Pioglitazone attenuates white matter injury in mice with cerebral ischemia-reperfusion
10.3760/cma.j.issn.1673-4165.2022.07.004
- VernacularTitle:吡格列酮减轻脑缺血再灌注小鼠脑白质损伤
- Author:
Rongliang WANG
1
;
Feng YAN
;
Yilin WANG
;
Yumin LUO
;
Shubei MA
Author Information
1. 首都医科大学附属宣武医院脑血管病研究室，北京 100000
- Keywords:
Brain ischemia;
Reperfusion injury;
Pioglitazone;
White matter;
Neuroprotective agents;
Disease models, animal;
Mice
- From:
International Journal of Cerebrovascular Diseases
2022;30(7):500-507
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of pioglitazone on white matter injury after cerebral ischemia-reperfusion in mice and its mechanism.Methods:Forty-two young male C57BL/6J mice were randomly divided into sham operation group, model group, and pioglitazone group ( n=14 in each group). The model of cerebral ischemia-reperfusion was induced by transient middle cerebral artery occlusion with suture-occluded method. On the 3 rd and 7 th day after the establishment of the model, the neural function was assessed by the adhesive removal test. The mice were killed on the 7 th day after the establishment of the model. HE staining was used to detect the extent of cerebral infarction. Immunofluorescence staining and Western blot analysis were used to detect the degree of white matter damage and the changes of microglia phenotype. Results:On the 7 th day after cerebral ischemia-reperfusion, the adhesive removal time in the PGZ group was significantly shortened compared with the model group ( P<0.05), the percentage of cerebral infarction volume was significantly reduced ( P<0.05), the ratio of MBP/NF200 fluorescence intensity in the cortical and striatal areas was significantly increased (all P<0.05), and the number of CD16 +/Iba1 + microglia was significantly decreased ( P<0.01), while the number of CD206 +/Iba1 + microglia tended to increase, but there was no statistical difference. Conclusion:Pioglitazone may reduce the degree of white matter injury and nerve function damage in mice with cerebral ischemia-reperfusion, and its mechanism may be associated with regulating the transformation of microglia from M1 type to M2 type.
