Protective effect of sodium butyrate on cerebral ischemia-reperfusion injury in mice
10.13699/j.cnki.1001-6821.2017.21.015
- VernacularTitle:丁酸钠对小鼠脑缺血再灌注损伤的保护作用
- Author:
Yi-Jun ZHUANG
1
;
Qiu-Xia XU
;
Yin ZHANG
;
Ya-Lan ZHANG
Author Information
1. 福建医科大学附属第二医院药学部
- Keywords:
cerebral ischemia-reperfusion injury;
sodium butyrate;
inflammatory reaction
- From:
The Chinese Journal of Clinical Pharmacology
2017;33(21):2143-2145,2157
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective mechanism of sodium butyrate on inflammatory response and neuronal apoptosis in mice with acute cerebral ischemia-reperfusion injury.Methods A total of 124 ICR mice were randomly divided into 4 groups (n =31):sham-operated group,model group,low-dose group (sodium butyrate at a dose of 5 mg · kg-1) and high-dose group (sodium butyrate at a dose of 10 mg· kg-1);The rat model of middle cerebral artery occlusion was established using the modified Zea-Longa suture method (after a 2 h-blood flow blocking,string-fastening device was removed to induce reperfusion).Sham operation group:bilateral common carotid arteries in mice were exposed without vascular ligation,and then skin was sutured.On the basis of the sham group,the model group,the low-dose group and the high-dose group received bilateral common carotid artery ligation (untied 30 min later),and gavage treatment 2 h after reperfusion.The mice in each group were sacrificed at 24 h after operation.WST-1 was used to detect superoxide dismutase (SOD) activity,the level of malonyldialdehyde (MDA) was measured by thiobarbituric acid (TBA);The expression of B-cell lymphoma-2 (Bcl-2),Bcl-2 Associated X (Bax),serine/threoninekinase (Akt) and phosphorylated Akt (p-Akt) protein in the brain tissue of mice were determined by Western blot;The levels of IL-8,IL-1 β and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA).Results After treatment,the levels of SOD in model group,sham-operated group and high-dose experimental group were (115.46 ± 25.07) (153.65 ± 34.81) (146.88±15.63) U·mg-1,MDAwere(2.13±0.27),(1.42±0.07),(1.43±0.08)nmol·mg-1;The levels of IL-13 in the model group,sham-operation group and high--dose group were (17.82 ± 3.60) (7.64 ± 1.14) (10.15 ±2.05) pg·mg-1,TNF-αwere (16.03±1.67),(7.95±0.85),(11.08±0.83) pg·mg-1,IL-8 were (15.03±2.66) (9.52±1.05) (10.28±1.17) pg · mg-1;The Bax/Bcl-2 ratios of the model group,the sham-operated group and the high-dose group were(0.67 ±0.05),(1.00 ±0.00),(1.13 ±0.10);The p-Akt/Akt ratios were (0.72 ±0.06),(1.00 ±0.00),(1.18 ±0.12);Statistically significant differences were found in all the parameters above between the model group and the sham-operated group/high-dose group (P ＜ 0.05).Conclusion Sodium butyrate was able to inhibit the apoptosis of neurons by suppressing inflammatory factors and oxidative stress,increasing the protein expression of Bcl-2 while decreasing that of Bax.
