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Apoptosis of lung cells regulated by JNK signal pathway in hyperoxia-induced lung injury
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- Author:
- No author available
- Journal Title:
- JOURNAL OF THE FOURTH MILITARY MEDICAL UNIVERSITY
- Issue:
- 12
- DOI:
- 10.3321/j.issn:1000-2790.2008.12.004
- Key Word:
- c-Jun氨基末端激酶;氧/毒性;肺/损伤;细胞凋亡
Abstract： 目的:观察高氧暴露下肺组织细胞凋亡和磷酸化c-Jun氨基末端激酶(p-JNK)蛋白表达的变化,并探讨JNK信号转导通路对高氧诱导的肺细胞凋亡的调控机制.方法: 48只3 wk龄Wistar大鼠随机分为空气对照组、高氧暴露3,7,14d组、空气+JNK抑制剂干预组、高氧暴露7 d+JNK抑制剂干预组.光镜下观察肺组织病理学改变,末端标记法(TUNEL)分析肺组织细胞凋亡的变化,免疫组化检测肺组织p-JNK的表达分布,Western Blot检测肺组织p-JNK蛋白质的表达含量.结果: 与空气对照组比较,高氧暴露各时间点组肺组织出现典型急、慢性肺损伤的病理学改变,肺组织细胞凋亡指数和p-JNK蛋白表达含量均显著增加(P<0.05),肺组织p-JNK阳性细胞明显增多.JNK抑制剂SP600125在空气和高氧暴露下均能明显阻断JNK的激活(P<0.05),SP600125干预后高氧暴露肺组织细胞凋亡指数显著减少(P<0.05).结论: 细胞凋亡是高氧肺损伤的一个重要病理组织学特点.JNK信号转导通路在高氧肺损伤中被激活,可能发挥促细胞凋亡效应.
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