CAJ | 학술논문

目的：探讨参希胶囊对内毒素血症小鼠心脏的保护作用。方法实验小鼠分为4组：对照组、模型组、参希组、参希＋模型组，采用腹腔注射内毒素（LPS）制备小鼠内毒素血症模型，对照组和参希组不予腹腔注射 LPS。参希组及参希＋模型组于造模前28 d 给予参希胶囊（0．75 g／kg）灌胃，余组给予等体积的生理盐水灌胃。分别于造模后6 h 行超声心动图测定心功能，检测心肌 TNF-α、IL-1β和 MDA 的含量，测定 SOD 的活性。结果与对照组比较，模型组小鼠的左室射血分数（EF）和短轴缩短率（FS）明显降低（P ＜0．05），参希预处理显著提高内毒素血症小鼠的 EF 和 FS 值（P ＜0．05）；与对照组比较，模型组小鼠心肌 TNF-α、IL-1β和 MDA 含量升高，SOD 的活性降低（P ＜0．05），参希预处理显著减少内毒素血症小鼠心肌 TNF-α、IL-1β和 MDA 含量，提高 SOD 的活性（P ＜0．05）。结论参希胶囊对内毒素血症小鼠心脏具有保护功能，其可能与降低心脏炎症因子水平和氧化应激反应有关。
목적：탐토삼희효낭대내독소혈증소서심장적보호작용。방법실험소서분위4조：대조조、모형조、삼희조、삼희＋모형조，채용복강주사내독소（LPS）제비소서내독소혈증모형，대조조화삼희조불여복강주사 LPS。삼희조급삼희＋모형조우조모전28 d 급여삼희효낭（0．75 g／kg）관위，여조급여등체적적생리염수관위。분별우조모후6 h 행초성심동도측정심공능，검측심기 TNF-α、IL-1β화 MDA 적함량，측정 SOD 적활성。결과여대조조비교，모형조소서적좌실사혈분수（EF）화단축축단솔（FS）명현강저（P ＜0．05），삼희예처리현저제고내독소혈증소서적 EF 화 FS 치（P ＜0．05）；여대조조비교，모형조소서심기 TNF-α、IL-1β화 MDA 함량승고，SOD 적활성강저（P ＜0．05），삼희예처리현저감소내독소혈증소서심기 TNF-α、IL-1β화 MDA 함량，제고 SOD 적활성（P ＜0．05）。결론삼희효낭대내독소혈증소서심장구유보호공능，기가능여강저심장염증인자수평화양화응격반응유관。
ABSTRACT:OBJECTIVE To explore the protective effects of shenxi on heart in endotoxemic mice.METHODS The experi-mental mice were equally and randomly divided into control group,LPS group,shenxi group,shenxi+LPS group.The endo-toxemia model was established by intraperitoneally injecting LPS.Mice in groups shenxi and shenxi+LPS were intragastrically administered with shenxi solution(0.75 g/kg),while the same dose of normal saline were intragastrically administrated in con-trol group and LPS group.The heart function was detected with echocardiography,and TNF-α,IL-1β,MDA,SOD in myocar-dial tissue was estimated 6 hours after LPS administration.RESULTS Compared with control group,LPS treatment could re-sult in decreased myocardial activities of SOD,and elevated levels of TNF-α,IL-1β,MDA(P <0.05);shenxi treatment could improve the above aberrant indices.Compared with control group,LPS treatment could result in reduced cardiac function, while shenxi treatment could improve it.CONCLUSION Shenxi shows a good cardio-protective effect on the cardiac injury in endotoxemic mice,which may be reached by suppressing inflammatory infiltration and oxidative stress reaction.