Inhibition effect of ubiquitin carboxy terminal hydrolase LI on cerebral ischemia/reperfusion injury in mice
10.16098/j.issn.0529-1356.2021.04.007
- Author:
Zhi-Feng PENG
1
;
Chen-Xu LI
1
;
Guo-Ying MA
1
;
Jing-Hui YANG
1
Author Information
1. Department of Physiology, Medical College of Shanxi Datong University
- Publication Type:Journal Article
- Keywords:
2;
3;
5-triphenyl tetrazolium chloride staining;
Ischemia/reperfusion injury;
Mouse;
Neurobehavioral score;
RT-PCR;
Ubiquitin carboxy terminal hydrolase LI;
Western blotting
- From:
Acta Anatomica Sinica
2021;52(4):543-553
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of inhibition of ubiquitin carboxy terminal hydrolase LI (UCHL1) on cerebral ischemia/reperfusion injury in mice. Methods Male BALB/c mice were randomly divided into sham group, ischemia/reperfusion (I/R) group, UCHL1 small interfering RNA (siRNA)group and scramble siRNA (control) group, 10 mice in each group. I/R model was established by reperfusion 24 hours after middle cerebral artery occlusion (MCAO) 60 minutes. In the siRNA group and control group, 10 JJLI UCHL1 siRNA or scramble siRNA was injected into the brain through the lateral ventricle 24 hours before MCAO. The expression of UCHL1 was detected by RT-PCR and Western blotting; the volume of cerebral infarction and the rate of edema were assessed by 2, 3, 5-triphenyl tetrazolium chloride (TTC) staining; and the score of neurological symptoms was assessed by neurobehavioral scoring. Results Compared with the sham group, the level of UCHL1 mRNA and protein in ischemic penumbra of I/R group were significantly higher (P< 0.05), while the expression of UCHL1 protein and mRNA in siRNA group were significantly lower (P< 0.05); at the same time, the volume of cerebral infarction, edema rate and neurobehavioral damage in I/R group increased significantly, while the volume and edema rate of cerebral infarction and neurobehavioral damage in siRNA group further increased (P< 0.05). Conclusion Inhibition of UCHL1 can aggravate the cerebral ischemia/reperfusion injury in mice, suggesting that the induction of UCHL1 after MCAO has a protective effect on the cerebral ischemia/reperfusion injury in mice.
