中风与神经疾病杂志2024，Vol.41Issue(9)：806-810,5.DOI:10.19845/j.cnki.zfysjjbzz.2024.0154
靶向TRIM63调节氧化应激通路改善急性脑卒中后血脑屏障损伤和神经功能恢复
Targeting TRIM63 to regulate oxidative stress pathways and improve blood-brain barrier injury and neurological recovery after acute stroke
摘要
Abstract
Objective To investigate the effect of targeting TRIM63 in regulating oxidative stress pathways and im-proving blood-brain barrier injury and neurological recovery after acute stroke.Methods Adult male C57 mice were ran-domly divided into Sham group,Vehicle group,and Myomed-205 group,and a mouse model of transient middle cerebral artery occlusion(tMCAO)was constructed.After removal of the suture,the mice in the Myomed-205 group and the Ve-hicle group were given intraperitoneal injection of TRIM63 inhibitor,and those in the Sham group were given intraperito-neal injection of an equal volume of solvent.On day 3 of reperfusion,TTC staining was used to observe cerebral infarct vol-ume,neurological score was used to evaluate neurological recovery,and the dry-wet weight method was used to measure brain water content.Reactive oxygen species(ROS),superoxide dismutase(SOD),glutathione(GSH),and malondial-dehyde(MDA)kits were used to measure the content of oxidative stress indices in brain.The Evans Blue method was used to observe blood-brain barrier injury,and Western blotting was used to measure the protein expression levels of ZO-1 and Occludin.Results Compared with the Vehicle group,the Myomed-205 group had a significant reduction in cerebral infarct volume(P<0.05),and compared with the control group,the 100 mg/ml Myomed-205 treatment group had signifi-cant reductions in neurological score(P<0.05)and brain water content(P<0.05).Compared with the Vehicle group,the Myomed-205 group had a significant reduction in the number of ROS-positive cells on days 3,7,and 14 after stroke(P<0.05),and compared with the control group,the Myomed-205 group had a significant reduction in the expression level of the pro-oxidative stress index MDA(P<0.05)and significant increases in the expression levels of the antioxidant indices GSH and SOD(P<0.05).Compared with the Vehicle group,the Myomed-205 group had a significant reduction in EB leakage on days 7 and 14 after stroke(P<0.05)and significant increases in the protein expression levels of ZO-1 and Occludin(P<0.05).Conclusion Inhibition of the TRIM63 signaling pathway can promote neurological recovery after cerebral ischemic stroke in mice,which may be achieved by alleviating oxidative stress and blood-brain barrier injury.关键词
TRIM63/氧化应激/血脑屏障/脑卒中Key words
TRIM63/Oxidative stress/Blood-brain barrier/Stroke分类
医药卫生引用本文复制引用
周静,温昌明,高军,张东焕,余洋,汪宁,张在行,张保朝..靶向TRIM63调节氧化应激通路改善急性脑卒中后血脑屏障损伤和神经功能恢复[J].中风与神经疾病杂志,2024,41(9):806-810,5.基金项目
河南省重点研发与推广专项(科技攻关)(202102310079) （科技攻关）
