CAJ | 학술논문

目的：探讨前列腺素 E1(PGE1)对肺撞击伤后肺泡细胞凋亡的影响。方法雄性 SD大鼠分为正常对照组、伤后对照组和伤后 PGE1处理组。致伤后24 h 检测动脉氧分压、肺系数,TUNEL 染色检测肺泡细胞凋亡的整体情况。以蛋白免疫印迹试验(Western blot)检测自噬相关蛋白及自噬调节蛋白 NIX 的表达情况。结果伤后24 h 肺组织可见明显结构破坏及肺水肿。与正常对照组相比,伤后对照组动脉氧分压降低(P <0.05),肺泡细胞凋亡指数增加(P <0.05),同时肺组织自噬相关蛋白Beclin-1、LC3Ⅱ/LC3Ⅰ及自噬调节蛋白 NIX 表达增加(P <0.05)。伤后 PGE1处理组动脉氧分压低于正常对照组(P <0.05),但较伤后对照组显著改善(P <0.05)；肺泡细胞凋亡指数高于正常对照组,但显著低于伤后对照组(P <0.05)；肺组织自噬相关蛋白Beclin-1、LC3Ⅱ/LC3Ⅰ及自噬调节蛋白 NIX 的表达虽然较正常对照组增加(P <0.05),但显著低于伤后对照组(P <0.05)。结论PGE1减轻大鼠肺撞击伤后肺泡细胞凋亡,此作用可能是通过抑制 NIX 介导的细胞自噬,以及肺泡细胞自噬性凋亡实现。
목적：탐토전렬선소 E1(PGE1)대폐당격상후폐포세포조망적영향。방법웅성 SD대서분위정상대조조、상후대조조화상후 PGE1처리조。치상후24 h 검측동맥양분압、폐계수,TUNEL 염색검측폐포세포조망적정체정황。이단백면역인적시험(Western blot)검측자서상관단백급자서조절단백 NIX 적표체정황。결과상후24 h 폐조직가견명현결구파배급폐수종。여정상대조조상비,상후대조조동맥양분압강저(P <0.05),폐포세포조망지수증가(P <0.05),동시폐조직자서상관단백Beclin-1、LC3Ⅱ/LC3Ⅰ급자서조절단백 NIX 표체증가(P <0.05)。상후 PGE1처리조동맥양분압저우정상대조조(P <0.05),단교상후대조조현저개선(P <0.05)；폐포세포조망지수고우정상대조조,단현저저우상후대조조(P <0.05)；폐조직자서상관단백Beclin-1、LC3Ⅱ/LC3Ⅰ급자서조절단백 NIX 적표체수연교정상대조조증가(P <0.05),단현저저우상후대조조(P <0.05)。결론PGE1감경대서폐당격상후폐포세포조망,차작용가능시통과억제 NIX 개도적세포자서,이급폐포세포자서성조망실현。
Objective To investigate the effect of prostaglandin E1 (PGE1)on alveolar cells apoptosis in rat lung impact in-jury model.Methods SD rats were divided into 3 groups (normal control group,lung injury control group and PGE1 treated group).PaO2 and pulmonary coefficient were detected after 24 h of impact.TUNEL labeling was used to evaluate apoptosis and Western blot was used to estimate protein expression levels of beclin-1,LC3 Ⅱ/LC3 Ⅰand NIX.Results After 24 h of impacting, there were obvious structural damage and pneumonedema in rat lung.Compared to normal control group,the PaO2 of lung injury control group decreased and the apoptosis of alveolar cells increased significantly(P <0.05).Furthermore,the expression levels of Beclin-1,LC3Ⅱ/LC3Ⅰ and NIX in the impacting control group were increased (P <0.05 ).In the PGE1 treated group,the PaO2 were decreased compared to normal control group(P <0.05),but these expression levels were higher significantly than lung injury control group (P <0.05).The expression levels of apoptosis,Beclin-1,LC3Ⅱ/LC3Ⅰ and NIX in the PGE1 treated group were in-creased compared to normal control group(P <0.05),but these expression levels were lower significantly than lung injury control group (P <0.05).Conclusion PGE1 could alleviate alveolar cells apoptosis after lung impacting injury,and which effect may as-cribe to PGE1 inhibiting NIX-mediated autophagy and autophagic apoptosis of alveolar cells.