Mechanisms of miR-24 inhibiting brain injury in rats with cerebral infarction through PI3K/AKT
10.19845/j.cnki.zfysjjbzz.2023.0027
- VernacularTitle:miR-24通过PI3K/AKT抑制脑梗死大鼠脑损伤的机制研究
- Author:
Keru ZHANG
1
;
Hua LI
1
Author Information
1. Department of Neurology,Shaanxi Hanzhong 3201 Hospital,Hanzhong 723000,China
- Publication Type:Journal Article
- Keywords:
miR-24;
Cerebral infarction;
PI3K/AKT;
Phosphorylation
- From:
Journal of Apoplexy and Nervous Diseases
2023;40(2):109-112
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism of miR-24 inhibiting brain injury in rats with cerebral infarction through PI3K/AKT signaling pathway.Methods Rats were divided into control group (n=10),sham group (n=10),model group (n=10) and experimental group (n=10).The middle cerebral artery occlusion method was used to establish the rat model of cerebral infarction.The sham group underwent the same operation without middle cerebral artery occlusion.The experimental group received stereotactic injection of miR-24 agomiR after modeling.HE staining was used to detect the pathological changes of cortex,TTC staining was used to detect the cerebral infarction area,qPCR was used to detect the expression level of miR-24 in brain tissue.Western blot was used to detect the expression of caspase-3,Bax and Bcl-2 in brain tissue,and the expression of PI3K,AKT and p-AKT were detected as well.Results Compared with the control group and the sham group,the neurological damage and pathological score of the model group was increased,and the neurological damage and pathological score of the miR-24 group was decreased.TTC staining showed that compared with the control group and the sham group,the cerebral infarction area of the model group was increased,and the cerebral infarction area of the miR-24 group was decreased,miR-24 in the model group was significantly decreased,while it was significantly increased in the experimental group (P<0.05).Western blot results showed that the expression of caspase-3 and Bax in the model group was significantly increased (P<0.05),and Bcl-2 was significantly decreased.The expression of caspase-3 and Bax in the experimental group was significantly decreased,and Bcl-2 was significantly increased (P<0.05).PI3K,AKT and p-AKT decreased in the model group,while PI3K,AKT and p-AKT increased in the experimental group (P<0.05). Conclusion MiR-24 can inhibit brain injury in rats with cerebral infarction,and its mechanism may be related to the phosphorylation of PI3K/AKT signaling pathway.
- Full text:2024061722365411658Mechanisms of miR-24 inhibiting brain injury in rats with cerebral infarction through PI3K_AKT.pdf
