Protective effect of sodium butyrate on brain injury induced by pneumolysin of infantile rats
10.3760/cma.j.issn.1008-1372.2013.06.006
- VernacularTitle:正丁酸钠在肺炎链球菌溶血素致幼鼠脑损伤中的保护作用
- Author:
Xiaohui QIAO
;
Minghai HUANG
;
Qiaoer LUO
- Publication Type:Journal Article
- Keywords:
Butyric acids/therapeutic use;
Brain injuries/drug therapy;
Brain injuries/chemically induced;
Streptolysins/adverse effects;
High mobility group proteins;
NF-kappa B
- From:
Journal of Chinese Physician
2013;(6):740-743
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of sodium butyrate on brain injury induced by pneumolysin of infantile rats.Methods Ninety-six normal healthy 1-month-old Spragne-Dawley (SD) rats were randomly divided into three groups,including pneumolysin (PLY) group (n =32),in which rat was injected PLY via external carotid; Normal saline (NS) group (n =32),injected NS via external carotid; sodium butyrate (SB) group (n =32),after injecting PLY,immediately administrated SB via venous.In the injection the 24th h and 48th h,superior vena cava blood was taken,and the animals were sacrificed,and brain tissue samples were prepared.The brain water content (BWC) was recorded by measuring both wet and dry weight,the Evans blue (EB) level was measured by the formamide method.The serum levels of high mobility group protein B1 (HMGB1) and nuclear factor kappa B (NF-κB) were measured by enzyme-linked immunosorbent assay (ELISA).Results In PLY group,brain tissue BWC,EB level,and the blood level of HMGB1 and NF-κB were increased significantly compared with the NS group at each time point,the difference was statistically significant (P ＜ 0.05).These indices were lower in the SB group compared with PLY group,the difference was statistically significant (P ＜ 0.05).The positive correlation was gotten between HMGB1 and NF-κB,BWC,EB levels in the PLY group and SB group (r =0.817 ～0.917,P ＜ 0.05).Conclusions SB has neuroprotective effect in brain injury induced by PLY,which maybe relevant to inhibition of NF-κB activation and suppression of HMGB1 expression.
