Protetive effect of substance P on hyperoxia lung injury and its regulation
10.3969/j.issn.1671-8348.2014.21.021
- VernacularTitle:神经肽 P物质对高氧肺损伤的保护作用调控机制研究
- Author:
Qing LI
;
Shuhong XU
;
Wenlian LI
;
Yun HAN
;
Dan YANG
;
Shenglin YANG
;
Yingbo ZOU
;
Feng XU
;
Bo HUANG
- Publication Type:Journal Article
- Keywords:
hyperoxic lung injury;
JNK2;
substance P
- From:
Chongqing Medicine
2014;(21):2749-2752
- CountryChina
- Language:Chinese
-
Abstract:
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 .
