贝母素甲对急性肺损伤小鼠COX-2、PGE2以及NO时间表达的影响

An effect of the Peimine on COX-2, PGE2 and NO expression of mice with acute lung injury

目的:探讨贝母素甲对急性肺损伤小鼠COX-2、PGE2以及NO时间表达的影响。方法:80只昆明种小鼠体重(20±5)g,被随机分成正常组,模型组,阳性对照组(Dex组),贝母素甲(PM)低、中、高剂量组,腹腔注射戊巴比妥(40mg/kg)麻醉小鼠,模型组、Dex组及PM组小鼠给予气管内注射4 mg/kg LPS诱导,建立急性肺损伤模型。注入LPS前1h、12h、24h、36h和注入后12h、24h、36h,后5组动物分别给予生理盐水、10mg/kg盐酸地塞米松、0.1mg/kg PM溶液、1mg/kg PM溶液、10mg/kg PM溶液,正常组给予同等体积生理盐水。实验结束后分别用Real-time PCR和酶免疫吸附实验(ELISA)测定肺脏COX-2的m RNA水平和蛋白含量,用酶免疫吸附实验(ELISA)测定血液PGE2以及NO水平。结果:与正常组和Dex组比较,LPS注射后导致肺部明显的水肿和炎症细胞浸润等现象,显著增加了COX-2、PGE2以及NO的表达,提示LPS处理后能启动一系列信号转导机制,激活多种炎症细胞和效应细胞,释放大量炎症介质或细胞因子。与模型组比较,PM处理后LPS对肺泡细胞的破坏明显减轻,COX-2、PGE2以及NO含量显著降低,提示PM对ALI小鼠的肺脏具有保护作用。结论:PM处理后可以抑制COX-2表达和明显降低PGE2以及NO含量,从而对急性肺损伤起到保护作用。

Objective： To evaluate effects ofpeimine on COX-2, PGE2 and NO expression of mice with acute lung injury. Methods： 80 Kunming mice were randomly divided into the normal group, model group, positive control group （Dex group）, peimine （PM） low, middle and high dose groups. All mice were given intraperitoneal injection of pentobarbital （40mg/kg）, the model group, Dex group and PM groups were given LPS （4mg/kg） in trachea, to establish model of acute lung injury. In injection LPS before 1 hour, 12 hours, 24 hours, 36 hours and after 12 hours, 24 hours, 36 hours, the five groups were given normal saline, 10mg/kg dexamethasone hydrochloride, 0. lmg/kg PM solution and lmg/kg PM solution, 10mg/kg PM solution respectively. The normal group was given normal saline. The mRNA levels and protein of COX-2 were measured byreal-time PCR and ELISA; and the levels of PGE2 and NO were measured by ELISA. Results： Compared with the normal group and the Dex group, LPS injection can cause the phenomenon of pulmonary edema and inflammatory cell, increase COX-2, PGE2 and NO expression. So after LPS treatment, a series of signal transduction mechanism was start; the inflammatory cells and effector cells were activated; mediators of inflammation and cell factor were released. Compared with the model group, after PM treatment, the destruction of alveolar cell was significantly reduced; the content of COX-2, PGE2 and NO was significantly decreased. So PM shows a protective effect on lung of ALI mice. Conclusion： PM can inhibit the expression of COX-2, significantly reduce the content of PGE2 and NO, and shows a protective effect on acute lung injury.