Effect and mechanism of β-1,3-galactosyltransferase 2 on brain injury in cerebral ischemic injury mice model
10.12007/j.issn.0258-4646.2024.08.011
- VernacularTitle:β-1,3-半乳糖基转移酶2对脑缺血损伤模型小鼠脑损伤的作用及其机制
- Author:
Fengyuan MA
1
;
He DIAO
;
Yue GU
;
Liansheng LU
;
Lijie FAN
;
Peng WANG
Author Information
1. 锦州医科大学 口腔医学院口腔修复科,辽宁 锦州 121000
- Keywords:
β-1,3-galactosyltransferase 2;
cerebral ischemic injury mice model;
brain injury
- From:
Journal of China Medical University
2024;53(8):736-740
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role of β-1,3-galactosyltransferase 2(B3galt2)in mice with cerebral ischemic injury.Methods Adult male C57BL/6J mice were randomly divided into the sham,suture-occluded middle cerebral artery occlusion(MCAO)model,MCAO model+lentiviral vector control(LV-GFP),and MCAO model+lentiviral vector overexpression B3galt2(LV-B3galt2)groups,with six mice in each group.Neurological deficit scoring and rotating rod experiments were performed 24 h after ischemia in each group,and 2,3,5-triphenyltetrazolium chloride(TTC)staining was used to determine the infarction volume.The number of neurons in the ischemic cerebral cortex was determined in each group using Nissl staining.The levels of oxidative stress-related factors in the brain tissues were detected using the relevant kits.Results Compared with the sham group,the MCAO model group showed increased infarct volume and neurological deficits(P<0.05),significantly decreased number of neurons in the ischemic cerebral cortex and levels of super-oxide dismutase(SOD)and glutathione peroxidase(GSH)(all P<0.05),and significantly increased levels of reactive oxygen species(ROS)and malondialdehyde(MDA)(all P<0.05).Compared with the MCAO model group,the LV-B3galt2 group had reduced volume of cerebral infarction,significantly improved neurological deficits(all P<0.05),significantly increased number of neurons in the ischemic cerebral cortex of mice,significantly decreased levels of ROS and MDA(P<0.05),and significantly elevated levels of SOD and GSH(all P<0.05).Conclusion B3galt2 overexpression can reduce brain injury in an ischemic damage mouse model,and its mechanism may be through the inhibition of oxidative stress reactions.
