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目的:观察丙酮酸乙酯(EP)对内毒素性急性肺损伤(ALI)大鼠肺组织核转录因子-κB(NF-κB)p65表达及肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)含量的影响,探讨EP可能的肺保护机制。方法:雄性SD大鼠30只随机分为三组(n均=10):正常对照组,静脉注射与其它二组等量生理盐水;LPS组,静脉注射脂多糖(LPS)5mg/kg复制大鼠ALI模型;EP+LPS组,于静脉注射LPS前1h腹腔内注射EP(40mg/kg)。所有动物于注射LPS或生理盐水后4h颈动脉放血处死,取肺组织用Westernblot测定其NF-κBp65的表达,用ELISA测定其TNF-α和IL-1β的含量。结果:与对照组相比,LPS组、EP+LPS组肺组织NF-κBp65表达增加,肺组织TNF-α和IL-lβ含量升高(P<0.05);与LPS组相比,EP+LPS组肺组织NF-κBp65表达降低,肺组织TNF-α和IL-lβ含量降低(P<0.05)。结论:EP通过下调大鼠LPS诱导的肺组织NF-κBp65表达,降低了TNF-α和IL-lβ的释放。EP可减轻ALI大鼠肺的炎症反应。
Objective: To observe the effect of ethyl pyruvate (EP) on the expression of NF-κB p65 and the levels of tumor necrosis factor-α (TNF-α) and interleukin- 1β (IL-1β) content of the impact of possible mechanism of pulmonary protection of EP. Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups (n = 10): normal control group, intravenous injection of normal saline and other two groups; LPS group, intravenous injection of lipopolysaccharide (LPS) 5mg / kg Rat ALI model; EP + LPS group, intraperitoneal injection of EP (40mg / kg) 1h before intravenous injection of LPS. All animals were sacrificed at 4h after carotid artery injection of LPS or saline, and the expression of NF-κBp65 in lung tissue was determined by Western blot. The contents of TNF-α and IL-1β were measured by ELISA. Results: Compared with the control group, the expression of NF-κBp65 in lung tissue increased and the content of TNF-α and IL-1β in lung tissue increased (P <0.05) in LPS group and EP + LPS group. Compared with LPS group, The expression of NF-κBp65 in the lung tissue decreased and the content of TNF-α and IL-1β in the lung tissue decreased (P <0.05). CONCLUSION: EP reduces the release of TNF-α and IL-1β by down-regulating the expression of NF-κBp65 in lung tissue induced by LPS in rats. EP attenuates lung inflammation in ALI rats.