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
Protective effect of sodium butyrate on brain injury induced by pneumolysin of infantile rats
摘要目的 探讨正丁酸钠(SB)对肺炎链球菌溶血素(PLY)致幼年大鼠脑损伤的保护作用.方法 96只1月龄SD大鼠按随机数字表法分为对照组(NS组,n=32),颈外动脉注射生理盐水;PLY脑损伤组(PLY组,n=32),颈外动脉注射PLY;SB治疗组(SB组,n=32),颈外动脉注射PLY后即刻静脉注射SB.于注射药物后24、48 h取上腔静脉血留取备用,并处死动物,制备脑组织标本,干湿质量法测定其脑组织含水量(BWC),甲酰胺法测定伊文思兰(EB)水平,采用酶联免疫吸附试验分析高迁移率族蛋白B1(HMGB1)、核转录因子(NF-κB)水平.结果 PLY组、SB组各时间点脑组织BWC、EB水平及血HMGB1、NF-κB水平均明显高于NS组(P<0.05),且SB组各时间点上述指标均低于PLY组(P<0.05).PLY组及SB组中HMGB1水平与NF-κB、BWC、EB水平呈正相关(r =0.817~0.917,P<0.05).结论 正丁酸钠可能通过抑制NF-κB活化减轻HMGB1的表达而对肺炎链球菌溶血素致脑损伤具有保护作用.
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abstractsObjective 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.
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