开口箭皂苷抗内毒素作用的实验研究

目的:探讨开口箭皂苷(STCB)对内毒素所致小鼠死亡的影响及其作用机制。方法:腹腔注射铜绿假单胞菌脂多糖(LPS)60 mg/kg或10 mg/kg分别制备昆明种小鼠内毒素中毒死亡模型和内毒素血症模型,STCB预防性灌胃给药,观察中毒小鼠存活率、存活时间;酶联免疫吸附测定法(ELISA)检测内毒素血症小鼠血清白介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)的含量。LPS刺激小鼠腹腔渗出细胞活化作为体外炎症模型,STCB干预,ELISA法检测培养上清IL-1β和TNF-α的含量。结果:经STCB(2004、00 mg/kg,连续5 d)预处理的动物存活率略高于模型组,但差异无统计学意义(P0.05),其存活时间显著长于模型组(P0.05)。经STCB(2004、00 mg/kg,连续5 d)预处理的动物血清IL-1β和TNF-α含量显著低于模型组(P0.05)。体外STCB(204、0μg/mL)明显抑制由LPS诱导的小鼠腹腔渗出细胞分泌IL-1β和TNF-α(P0.05)。结论:STCB对LPS中毒所致小鼠死亡有一定的保护作用,其机制可能与下调IL-1β和TNF-α分泌有关。

Study on the anti-endotoxin effect of saponin from Tupistra chinensis

Objective:To investigate the effect of saponin from Tupistra chinensis Baker(STCB)on lethal toxicity of endotoxin in mice and explore the underlying mechanism.Methods:Mouse models of endotoxin-induced death and endotoximia were established by intraperitoneal administration of KM mice with lipopolysaccharides(LPS)from Pseudomonas aeruginosa in doses of 60 mg/kg and 10 mg/kg respectively.Mouse survival rate and survival time were recorded and the serum levels of interleukin-1β(IL-1β)and tumor necrosis factor-α(TNF-α)in endotoximia mice were measured by enzyme-linked immunosorbent assay(ELISA).Mouse peritoneal exudate cells induced by LPS were used as an in vitro inflammatory model,which was then intervened with STCB and the levels of IL-1β and TNF-α in the culture supernatants were measured by ELISA.Results:The survival rates of mice prophylactically treated with STCB(200 and 400 mg/kg,in 5 consecutive days)were slightly higher compared with that in model group,but no statistical difference was observed(P>0.05).The survival time was much longer in the treated group(P<0.05).The serum levels of IL-1β and TNF-α in STCB-treated mice(200 and 400 mg/kg,in 5 consecutive days)were significantly lower compared with those in model group(P<0.05).STCB(20 and 40 μg/mL)remarkably inhibited LPS-induced IL-1β and TNF-α production by peritoneal exudate cells in vitro(P<0.05).Conclusion:Saponin from Tupistra chinensis showed beneficial effect on the prevention of mice from lipopolysaccharides-induced death,in which down regulation of IL-1β and TNF-α expression might be involved.