中国临床药理学杂志2017，Vol.33Issue(21)：2143-2145,2157,4.DOI:10.13699/j.cnki.1001-6821.2017.21.015
丁酸钠对小鼠脑缺血再灌注损伤的保护作用
Protective effect of sodium butyrate on cerebral ischemia-reperfusion injury in mice
摘要
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.关键词
脑缺血再灌注损伤/丁酸钠/炎症反应Key words
cerebral ischemia-reperfusion injury/sodium butyrate/inflammatory reaction分类
医药卫生引用本文复制引用
庄奕筠,许秋霞,张吟,张雅兰..丁酸钠对小鼠脑缺血再灌注损伤的保护作用[J].中国临床药理学杂志,2017,33(21):2143-2145,2157,4.基金项目
福建省科技厅社会发展引导性基金资助项目(2015Y0055) （2015Y0055）
福建省卫计委青年科研课题基金资助项目(2015-1-60) （2015-1-60）
