论文部分内容阅读
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 and mechanism of Skeletalis Saponins (STCB) on the death of mice induced by endotoxin. Methods: LPS (60 mg / kg or 10 mg / kg) were injected intraperitoneally to induce endotoxemia and endotoxemia in Kunming mice, respectively. STCB was given intragastrically for gavage. Survival rate and survival time of poisoned mice were measured. Serum levels of interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) in endotoxemia mice were detected by enzyme linked immunosorbent assay (ELISA). LPS stimulated peritoneal exudation in mice as an in vitro model of inflammation, STCB intervention, ELISA assay IL-1β and TNF-α content in culture supernatant. Results: The survival rate of animals pretreated with STCB (2004,00 mg / kg for 5 days) was slightly higher than that of the model group (P> 0.05), and the survival time was significantly longer than that of the model group (P < 0.05). The levels of IL-1β and TNF-α in serum pretreated with STCB (2004,00 mg / kg for 5 d) were significantly lower than those in model group (P <0.05). In vitro STCB (204,0μg / mL) significantly inhibited IL-1β and TNF-α secreted by LPS-induced mouse peritoneal exudate cells (P <0.05). Conclusion: STCB can protect mice from LPS poisoning to a certain extent, which may be related to down-regulation of IL-1β and TNF-α secretion.