CAJ | 학술논문

目的：观察JNK2信号途径在高氧肺损伤中的表达，探讨神经肽P物质（SP）在高氧肺损伤中的保护作用及机制。方法将16只早产SD大鼠分配给代母鼠并分为4组（每组n＝4）：空气加9 g/L盐水组（A组），空气加SP组（B组）、高氧加9 g/L盐水组（C组）、高氧加SP组（D组），B、D组予腹腔注射SP1×10-6 mol·L -1·kg -1·d-1，A、C组腹腔注射同等体积的9g/L盐水。实验14 d后，观察肺组织病理改变；并测定肺湿质量/干质量（W/D）值，肺组织中SP的水平；免疫组织化学观察增殖细胞核抗原（PCNA）表达和原位末端标记法（TUNEL）法观察肺组织细胞凋亡的情况；检测超氧化物歧化酶（SOD）、丙二醛（MDA）和谷胱甘肽（GSH）水平；用Western blot检测JNK2蛋白水平。结果与A组相比，高氧各组均有不同程度的肺损伤，但D组肺损伤较C组有所减轻。Western blot显示，C组JNK2水平明显高于A组；干预后，D组JNK2水平低于C组。各组肺W/D值、PCNA和TUNEL组织分布表达以及SOD、MDA和GSH的表达与JNK2蛋白水平变化趋势一致。结论高氧应激可激活损伤肺组织JNK2活性；SP对高氧肺损伤保护作用机制可能是通过下调高氧诱导的JNK2的激活以抑制氧化损伤实现的。
목적：관찰JNK2신호도경재고양폐손상중적표체，탐토신경태P물질（SP）재고양폐손상중적보호작용급궤제。방법장16지조산SD대서분배급대모서병분위4조（매조n＝4）：공기가9 g/L염수조（A조），공기가SP조（B조）、고양가9 g/L염수조（C조）、고양가SP조（D조），B、D조여복강주사SP1×10-6 mol·L -1·kg -1·d-1，A、C조복강주사동등체적적9g/L염수。실험14 d후，관찰폐조직병리개변；병측정폐습질량/간질량（W/D）치，폐조직중SP적수평；면역조직화학관찰증식세포핵항원（PCNA）표체화원위말단표기법（TUNEL）법관찰폐조직세포조망적정황；검측초양화물기화매（SOD）、병이철（MDA）화곡광감태（GSH）수평；용Western blot검측JNK2단백수평。결과여A조상비，고양각조균유불동정도적폐손상，단D조폐손상교C조유소감경。Western blot현시，C조JNK2수평명현고우A조；간예후，D조JNK2수평저우C조。각조폐W/D치、PCNA화TUNEL조직분포표체이급SOD、MDA화GSH적표체여JNK2단백수평변화추세일치。결론고양응격가격활손상폐조직JNK2활성；SP대고양폐손상보호작용궤제가능시통과하조고양유도적JNK2적격활이억제양화손상실현적。
Objective To investigate the expression of JNK2 in hyperoxic lung injury ,and explore the protective effect of sub-stance P (SP) on hyperoxic lung injury and its mechanism .Methods Sixteen SD rats were divided into four groups with 4 rats in each group :room-air and f 9 g/L saline group (group A) ,room-air and SP group (group B) ,hyperoxia injury group and f 9 g/L sa-line group (group C) ,hyperoxia injury group and SP group (group D) .Rats ingroup B and D were injected with SP 1 × 10-6 mol · L -1 · kg -1 · d-1 intraperitoneally ,group A and group C were injected with an equal volume of 9 g/L saline .The animals were sac-rificed after 14 days of experiment .Lung pathology was examined with light microscopy ,lung wet/dry (W/D) ratio and the level of SP and PCNA and TUNEL in lung were evaluated .The Superoxide dismutase (SOD) ,malondialdehyde (MDA) and glutathione (GSH) level were assayed respectively in lung tissue .The quanlity of JNK2 protein was detected by Western blot analysis .Results Compared with group A ,the high oxygen groups all had different degrees of lung injury ,,while the lung pathological pictures in group D was improved significantly compared with group C .Western blot showed that level of JNK2 in group C was obviously higher than that of group A ;After the intervention ,level of JNK2 in group D was lower than that of group C .The lung W/D retio , TUNEL and PCNA expression and distribution SOD ,MDA and GSH was consistent with the trends of JNK2 protein expression . Conclusion High oxygen stress can activate damage lung tissue JNK 2 activity ;SP protection mechanism of high oxygen lung injury may be induced by cutting high oxygen activation of JNK 2 to inhibit oxidative damage .