Neuroprotective effect and mechanism of levetiracetam on acute cerebral ischemia -reperfusion injury in mice
10.13699/j.cnki.1001-6821.2018.06.020
- VernacularTitle:左乙拉西坦对小鼠急性脑缺血再灌注损伤的神经保护作用及机制
- Author:
Jun-Rong LEI
1
;
Jun QIN
;
Lei MOU
;
De-Sheng WEI
;
Bo DUAN
Author Information
1. 湖北医药学院附属十堰市太和医院神经外科
- Keywords:
cerebrovascular disease;
levamisetan;
reperfusion injury;
B-lymphoma-2 gene-related X protein
- From:
The Chinese Journal of Clinical Pharmacology
2018;34(6):678-681
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the neuroprotective effect and mechanism of levofloxacin (LEV) on acute cerebral ischemia-reperfusion injury in mice.Methods A total of 30 C57BL/6J mices were randomly divided into sham operation group (n =6),experimental group (n =18) and control group (n =6).According to the intervention time,experimental group was divided into 0,3,6 h experimental group,6 mices in each group.The model of middle cerebral artery occlusion (MCAO) was established by modified Longa method,sham operation group did not block the middle cerebral artery,experimental group was given LEV 10 mg · kg-1 by tail vein at 0,3,6 h after modeling,sham opera tion group and control group were given 0.9％ NaC1.The neurological score was measured by Longa score;the infarct volume was measured by 2,3,5-triphenyte-trazoliumchloride (TTC) staining;the neuronal apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method,apoptosis index (AI) was calculated;the positive expression of B-lymphoma-2 gene-related X protein (Bax) and caspase-3 was detected by immunohistochemistry.Results The Longa scores in sham operation group,control group and 0,3,6 h experimental group were 0,(2.88 ± 1.03),(1.77 ± 0.56),(2.21 ± 0.96),(2.66 ± 1.03) points.Compared with control group,the Longa score of 0 h group was significantly reduced (P ＜ 0.05),but there was no significant difference among 0,3 and 6 h groups (P ＞ 0.05).The cerebral infarct volume in sham operation group,control group and 0,3,6 h experimental group were 0,(21.03 ± 0.25),(13.14 ± 0.44),(13.21 ± 0.53),(16.86 ± 0.65) mm3.The AI in sham operation group,control group and 0,3,6 h experimental group were 1.16 ±0.32,36.51 ±2.44,18.45 ±0.46,20.15 ±0.69,26.49 ±0.77.Compared with control group,the cerebral infarct volume and AI of experimental groups were significantly decreased (P ＜ 0.01).The cerebral infarct volume in 0,3 h experimental group were significantly lower than 6 h experimental group (P ＜0.01).The cerebral infarct volume and AI increased gradually with the prolong of LEV duration,and the difference was significant in 3 groups (P ＜ 0.01).The Bax in sham operation group,control group and0,3,6 h experimental group were 2.63 ±1.04,20.76±1.75,18.13 ±0.42,19.05 ±0.71,19.25 ±1.32,caspase-3 were 5.15 ±2.02,60.13 ±2.41,34.31±2.36,36.25 ±2.01,52.13 ±2.23.Compared with control group,the caspase-3 in experimental groups were significantly lower (P ＜0.05,P ＜0.01).The expression of caspasc-3 in mice gradually increased with the prolongation of LEV,there was no significant difference in Bax expression among 3 groups (P ＞ 0.05).Conclusion LEV can inhibit the expression of apoptotic protein Bax and caspase-3 after cerebral ischemia reperfusion injury,so as to inhibit the apoptosis of nerve cells and play a role in brain protection.
