摘要
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(P>0.05),其存活时间显著长于模型组(P<0.05)。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(P<0.05)。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(P<0.05)。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。
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 byintraperitoneal 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-1/3（IL-1/3） and tumor nec- rosis 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 -β 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 〈 O. 05 ）. The serum levels of IL-1/3 and TNF-ot in STCB-treated mice （200 and 400 mg/kg, in 5 consecutive days ）were significantly lower compared with those in model group （P 〈 O. 05 ）. STCB（20 and 40 μg/mL）remarkably inhibited LPS-induced IL-1/3 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 lipopolysacchar- ides-induced death, in which down regulation of IL-lfl and TNF-α expression might be involved.
出处
《中药材》
CAS
CSCD
北大核心
2012年第1期102-105,共4页
Journal of Chinese Medicinal Materials
基金
广东省自然科学基金(07005189)
