CAJ | 학술논문

目的：观察苦参素对内毒素性休克大鼠肾损伤的保护作用。方法将24只雄性Wistar大鼠随机分为正常组（8只）、内毒素性休克组（8只）和苦参素治疗组（8只），内毒素性休克组和苦参素治疗组从股静脉注射脂多糖（LPS，15 mg/kg）建立内毒素性休克模型，造模15 min后，苦参素治疗组自股静脉输注苦参素注射液，观察其对平均动脉压（MAP）影响，实验结束后取材测定血浆中反映肾功能指标的尿素（Urea）、肌酐（Cr）含量，及肾组织匀浆中炎症因子白介素（IL）-6、IL-10、肿瘤坏死因子-α（TNF-α）的含量。结果苦参素治疗可防止内毒素性休克大鼠MAP的进行性下降；内毒素性休克组大鼠血浆Urea、Cr含量显著高于正常组，肾组织内IL-6、IL-10和TNF-α明显上升，苦参素治疗组大鼠血浆Urea、Cr含量显著低于内毒素性休克组，肾组织内IL-6和TNF-α显著下降。结论苦参素可对内毒素性休克后的肾功能提供一定的保护作用，其机制可能与抑制肾内促炎性细胞因子释放有关。
목적：관찰고삼소대내독소성휴극대서신손상적보호작용。방법장24지웅성Wistar대서수궤분위정상조（8지）、내독소성휴극조（8지）화고삼소치료조（8지），내독소성휴극조화고삼소치료조종고정맥주사지다당（LPS，15 mg/kg）건립내독소성휴극모형，조모15 min후，고삼소치료조자고정맥수주고삼소주사액，관찰기대평균동맥압（MAP）영향，실험결속후취재측정혈장중반영신공능지표적뇨소（Urea）、기항（Cr）함량，급신조직균장중염증인자백개소（IL）-6、IL-10、종류배사인자-α（TNF-α）적함량。결과고삼소치료가방지내독소성휴극대서MAP적진행성하강；내독소성휴극조대서혈장Urea、Cr함량현저고우정상조，신조직내IL-6、IL-10화TNF-α명현상승，고삼소치료조대서혈장Urea、Cr함량현저저우내독소성휴극조，신조직내IL-6화TNF-α현저하강。결론고삼소가대내독소성휴극후적신공능제공일정적보호작용，기궤제가능여억제신내촉염성세포인자석방유관。
Objective To evaluate the protective effects of oxymatrine injection on rats with endotoxic shock. Methods Wistar rat model of endotoxic shock was produced in this study. Twenty-four Wistar rats were randomly divided into normal control group (n=8), endotoxic shock group (n=8) and oxymatrine injection treatment group (n=8). Fifteen min?utes after the infusion of LPS (15 mg/kg) from femoral vein, oxymatrine was injected from femoral vein in treatment group, then we observed the mean arterial pressure (MAP) for six hours. At the end of experiment blood samples were harvested for measurement of urea and creatinine (Cr), which reflect renal function. Also contents of IL-6, IL-10, TNF-αin the renal ho?mogenate were detected. Results Oxymatrine can prevent progressive decrease of MAP in endotoxin shock treatment group. The contents of plasma urea and Cr were significantly higher in endotoxin shock group than those of control group. The contents of IL-6, IL-10 and TNF-αin renal homogenate increased obviously, but after the injection of oxymatrine, the contents of urea and Cr significantly decreased in treatment group, also IL-6 and TNF-α were significantly declined. Conclusion Oxymatrine provides protection at renal function after endotoxin shock, and its mechanism may be related to inhibit the releasing of inflammatory cytokines in kidney.