湖北科技学院学报（医学版）
湖北科技學院學報（醫學版）
호북과기학원학보（의학판）
JOURNAL OF XIANNING UNIVERSITY (MEDICAL SCIENCES)
2015年
3期
185-187
,共3页
硫辛酸%内毒素%心肌损伤
硫辛痠%內毒素%心肌損傷
류신산%내독소%심기손상
Lipoic acid%Lipopolysaccharide%Myocardial injury
目的：以内毒素（ lipopolysaccharide ，LPS）诱导法建立全身炎症反应综合征（ SIRS）大鼠心肌损伤模型，探讨不同浓度硫辛酸（ lipoic acid，LA）对大鼠心肌损伤的保护作用。方法选择健康SD大鼠75只，其中60只腹腔注射内毒素25mg／kg，构建SIRS大鼠心肌损伤模型，再分为阴性对照组、LA大剂量组、LA中剂量组、LA小剂量组，每组15只；其余15只大鼠为正常组。分别于24、48、72h后采用real－time PCR检测各组每只大鼠心肌组织中核因子κB（nuclear factor kappa B，NF－κB）、白细胞介素1（interleukin 1，IL－1）水平，ELISA法检测肿瘤坏死因子（ tumor necrosis factor α，TNF－α）的水平。同时观察心肌组织变化。结果 LPS诱导后，LA阴性对照组大鼠心肌中NF－κB、IL－1、TNF－α在72 h时最高。与阴性对照组比较，处理24、48、72h后，LA大剂量组、中剂量组中NF－κB、IL－1、TNF－α表达水平下降（P＜0．05）；随硫辛酸剂量加大，心肌组织炎症反应相应减轻。结论硫辛酸对SIRS大鼠心肌损伤有一定保护作用，其机制可能与抑制NF－κB激活以及下调心肌组织中IL－1、TNF－α的表达有关。
目的：以內毒素（ lipopolysaccharide ，LPS）誘導法建立全身炎癥反應綜閤徵（ SIRS）大鼠心肌損傷模型，探討不同濃度硫辛痠（ lipoic acid，LA）對大鼠心肌損傷的保護作用。方法選擇健康SD大鼠75隻，其中60隻腹腔註射內毒素25mg／kg，構建SIRS大鼠心肌損傷模型，再分為陰性對照組、LA大劑量組、LA中劑量組、LA小劑量組，每組15隻；其餘15隻大鼠為正常組。分彆于24、48、72h後採用real－time PCR檢測各組每隻大鼠心肌組織中覈因子κB（nuclear factor kappa B，NF－κB）、白細胞介素1（interleukin 1，IL－1）水平，ELISA法檢測腫瘤壞死因子（ tumor necrosis factor α，TNF－α）的水平。同時觀察心肌組織變化。結果 LPS誘導後，LA陰性對照組大鼠心肌中NF－κB、IL－1、TNF－α在72 h時最高。與陰性對照組比較，處理24、48、72h後，LA大劑量組、中劑量組中NF－κB、IL－1、TNF－α錶達水平下降（P＜0．05）；隨硫辛痠劑量加大，心肌組織炎癥反應相應減輕。結論硫辛痠對SIRS大鼠心肌損傷有一定保護作用，其機製可能與抑製NF－κB激活以及下調心肌組織中IL－1、TNF－α的錶達有關。
목적：이내독소（ lipopolysaccharide ，LPS）유도법건립전신염증반응종합정（ SIRS）대서심기손상모형，탐토불동농도류신산（ lipoic acid，LA）대대서심기손상적보호작용。방법선택건강SD대서75지，기중60지복강주사내독소25mg／kg，구건SIRS대서심기손상모형，재분위음성대조조、LA대제량조、LA중제량조、LA소제량조，매조15지；기여15지대서위정상조。분별우24、48、72h후채용real－time PCR검측각조매지대서심기조직중핵인자κB（nuclear factor kappa B，NF－κB）、백세포개소1（interleukin 1，IL－1）수평，ELISA법검측종류배사인자（ tumor necrosis factor α，TNF－α）적수평。동시관찰심기조직변화。결과 LPS유도후，LA음성대조조대서심기중NF－κB、IL－1、TNF－α재72 h시최고。여음성대조조비교，처리24、48、72h후，LA대제량조、중제량조중NF－κB、IL－1、TNF－α표체수평하강（P＜0．05）；수류신산제량가대，심기조직염증반응상응감경。결론류신산대SIRS대서심기손상유일정보호작용，기궤제가능여억제NF－κB격활이급하조심기조직중IL－1、TNF－α적표체유관。
ABSTRACT:Objective To explore the protective effects of different dose of lipoic acid onmyocardial inju-ry rats with systemic inflammatory response syndrome ( SIRS) induced by lipopolysaccharide .Methods A total of 75 healthy SD rats were enrolled .Among them,60 rats were intraperitoneally injected with 25mg/kg LPS to establish SIRS model of myocardial injury ,thenthose rats were divided into negative control group ,LA high-dose group ,LA middle-dose group and LA low-dose group ,15 rats in each group .the other 15 rats were intraperitone-ally injected with saline solution ( normal group ) .The levels of NF-κB and IL-1 in myocardium were detected with real-time PCR after 24h,48h and 72h,respectively,and the level of TNF-αwas measured with ELISA.HE staining was used to observe the microscopical change of myocradium tissue .Results After challenge with LPS , the levels of NF-κB,IL-1 and TNF-αin myocardium in negative control group were the highest at 72h.Com-pared with the negative control group ,the levels of NF-κB,IL-1 and TNF-αin LA high-dose group and LA mid-dle-dose group were decreased after treatment for 24h,48h and 72h(P<0.05).With LA dose increase,myo-cardial tissue inflammation reduced accordingly .Conclusion Lipoic acid has a protective effect on myocardial injury of SIRS rats,and the underlyingmechnism may be correlated with inhibition of NF-κB activation and the down-regulation of IL-1 and TNF-αexpression .
