神经肽P物质对高氧肺损伤的保护作用调控机制研究

发布时间：2018-03-23 22:37

本文选题：高氧肺损伤　切入点：JNK　出处：《重庆医学》2014年21期

【摘要】：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9g/L盐水组(A组),空气加SP组(B组)、高氧加9g/L盐水组(C组)、高氧加SP组(D组),B、D组予腹腔注射SP 1×10-6 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14d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。
[Abstract]:Objective to observe the expression of JNK2 signal pathway in hyperoxia lung injury. To investigate the protective effect and mechanism of neuropeptide substance P (SP) on hyperoxia lung injury. Methods Sixteen preterm SD rats were divided into 4 groups (n = 4: air + 9g/L saline group, group A, air plus SP, group B, hyperoxia). Group C with 9g/L saline, group D with hyperoxia plus SP group D, group B were injected intraperitoneally with SP1 脳 10-6 mol L-1 kg-1 d-1An C group with 9g/L saline of the same volume. After 14 days of experiment, the same volume of 9g/L saline was injected into the control group. Lung tissue pathological changes were observed, lung wet / dry weight (WR / D) values and SP level in lung tissue were measured, and proliferating cell nuclear antigen (PCNA) expression and apoptosis in lung tissue were observed by immunohistochemical staining and Tunel in situ Nick end labeling (Tunel) method. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH) and JNK2 protein were detected by Western blot. The level of JNK2 in group C was significantly higher than that in group A. Western blot showed that the level of JNK2 in group C was significantly higher than that in group A. After intervention, the level of JNK2 in group D was lower than that in group C. the expression of JNK2 and GSH in lung tissue of each group was consistent with that of JNK2 protein. Conclusion Hyperoxia stress can activate the activity of JNK2 in injured lung tissue and SP on hyperoxia lung. The mechanism of injury protection may be the inhibition of oxidative damage by down-regulating the activation of hyperoxia-induced JNK2.
【作者单位】：贵州省遵义市第一人民医院儿童保健科;重庆医科大学附属儿童医院儿童重症医学科;
【基金】：贵州省卫生厅科学技术基金项目(gzwkj2011-1-092) 贵州省科学技术基金项目(黔科合J字[2011]2341号)
【分类号】：R563.8

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