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全氟化碳对脂多糖诱导Ⅱ型肺泡上皮损伤的保护机制研究
引用本文:朱月钮,陈菲,张明军,魏红霞,朱晓东.全氟化碳对脂多糖诱导Ⅱ型肺泡上皮损伤的保护机制研究[J].中国小儿急救医学,2014(5):288-291.
作者姓名:朱月钮  陈菲  张明军  魏红霞  朱晓东
作者单位:上海交通大学医学院附属新华医院小儿重症医学科,200092
基金项目:上海市卫生局课题(2009066)
摘    要:目的 探讨全氟化碳(perfluorocarbon,PFC)对脂多糖(lipopolysaccharide,LPS)作用下胎鼠Ⅱ型肺泡上皮细胞的凋亡以及炎症反应的影响。方法 分离纯化原代胎鼠Ⅱ型肺泡上皮细胞,采用随机数字表法随机分为对照组、LPS组、PFC组、PFC+ LPS组.LPS组培养液加入1μg/ml的LPS,PFC组培养液加入20%容积比的PFC,PFC+ LPS组培养液加入1μg/ml LPS和20%容积比PFC,共同培养后lh后,电镜观察Ⅱ型肺泡上皮细胞的形态学变化,流式细胞仪鉴定各组细胞凋亡率,用ELISA方法检测各组细胞培养上清液中白细胞介素(interleukin,IL)-6及IL-10的浓度.结果 LPS组Ⅱ型肺泡上皮细胞凋亡率(14.29±1.93)%显著高于对照组(10.89±1.04)%,差异有统计学意义(P<0.05);PFC+ LPS组Ⅱ型肺泡上皮细胞凋亡率(12.22±1.47)%显著低于LPS组(P <0.05);LPS组IL-6浓度(482.58 ±26.84) pg/ml]显著高于对照组(229.40 ±7.61) pg/ml] (P <0.05),加入PFC后可显著减少LPS诱导的IL-6合成(265.44 ±29.95) pg/ml] (P <0.05);LPS组IL-10浓度(1 497.29±191.89) pg/ml]显著高于对照组(725.87 ±51.83) pg/ml] (P <0.05),加入PFC对LPS诱导的IL-10合成无影响(P>0.05)。结论 PFC可有效减轻脂多糖诱导的胎鼠Ⅱ型肺泡上皮细胞的炎性损伤,并减轻炎症反应的程度。

关 键 词:全氟化碳  肺泡上皮细胞  脂多糖  凋亡  炎症因子

The protective effect of perfluorocarbon on the injury of alveolar epithelial cells induced by lipopolysaccharide
Zhu Yueniu,Chen Fei,Zhang Mingjun,Wei Hongxia,Zhu Xiaodong.The protective effect of perfluorocarbon on the injury of alveolar epithelial cells induced by lipopolysaccharide[J].Chinese Pediatric Emergency Medicine,2014(5):288-291.
Authors:Zhu Yueniu  Chen Fei  Zhang Mingjun  Wei Hongxia  Zhu Xiaodong
Institution:( PICU , Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China)
Abstract:Objective To explore the effects of perfluorocarbon (PFC) on the damaged type Ⅱ alveolar epithelial cells (AEC Ⅱ) induced by lipopolysaccharide (LPS),and the apoptosis and inflammatory reaction of AEC Ⅱ induced by LPS.Methods Primary AEC Ⅱ was divided into control group according to the random number table method,LPS group,PFC group and PFC + LPS group.LPS group:LPS (1 μg/ml) was added to cells.PFC group:PFC (20%) was added to cells.PFC + LPS group:PFC (20%) and LPS (1 μg/ml) were added to cells.The apoptotic rate of AEC Ⅱ was detected by flow cytometry.Morphologic change was observed by electron microscope.Concentrations of intedeukin (IL)-6 and IL-10 of supernatant were detected by ELISA.Results Apoptotic rate of AEC Ⅱ remarkably increased in LPS group than in control grouop (10.89 ± 1.04) % vs (14.29 ± 1.93) %] (P < 0.05).Compared with LPS group,the apoptotic rate of AEC Ⅱ decreased remarkably in the PFC + LPS group (12.22 ± 1.47) %],(P < 0.05).IL-6 production of AEC Ⅱ significantly increased in LPS group than in control group (482.58 ± 26.84) vs (229.40 ± 7.61) pg/ml pg/ml] (P < 0.05),while decreased in PFC + LPS group (265.44 ± 29.95) pg/ml].IL-10 production of AEC Ⅱ significantly increased in LPS group than in control group (1 497.29 ±191.89) pg/ml vs (725.87 ±51.83) pg/ml] (P <0.05),while there was no difference between LPS group and PFC + LPS group (P > 0.05).Conclusion PFC can protect AEC Ⅱ against the injury induced by LPS.PFC can also release the level of inflammatory response.
Keywords:Perfluorocarbon  Alveolar epithelial cell  Lipopolysaccharide  Apoptosis  Inflammatory factor
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