MEDLINE/PubMed Journal Browser Search

Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

Title: [Role and mechanism of hydrogen sulfide in cigarette smoke induced chronic obstructive pulmonary disease related pulmonary vascular remodeling in rats].
Author: Li MX, Chen YH, Liao CC, Lin F, Bai Y, Mi WJ, Sun Y, Qi YF.
Journal: Zhonghua Yi Xue Za Zhi; 2017 Jan 10; 97(2):137-142. PubMed ID: 28088960.
Abstract:
Objective: To investigate the role and mechanism of hydrogen sulfide (H₂S) in rats with chronic obstructive pulmonary disease (COPD) related pulmonary vascular remodeling. Methods: Twenty four healthy male Sprague-Dawley rats were randomly divided into 4 groups: control group, cigarette smoke (CS) group, CS+ Sodium hydrosulfide (NaHS) group and CS+ DL-propargylglycine (PPG) group. Rats in control group were fed normally and breathed clear air, and for the rest groups, passive cigarette smoke inhalation method were adopted to establish COPD model. After 8 weeks, the rats in corresponding groups were treated by NaHS or PPG. After 16 weeks, the markers of pulmonary vascular remodeling in all groups were measured. Proliferation marker proliferative cell nuclear antigen (PCNA) and oxidative stress marker 3-neurotrophin (3-NT) in all groups were measured by immunohistochemistry (IHC). Results: Compared with control group, the airway resistance was increased (0.859±0.283 vs 0.578±0.088, P<0.05) and the pathological scores was much higher in CS group, which suggested that the COPD model was successful. The degree of small resistance pulmonary artery medial wall thickness and full vascular muscularization of CS group were much higher (0.54±0.20 vs 0.37±0.12, 0.39±0.08; 0.61±0.16 vs 0.20±0.12, 0.34±0.13, all P<0.01)than control group and CS+ NaHS group, there was no significant difference between CS+ PPG group and CS group. In accordance with the results of morphometric analysis, the proliferation marker PCNA was more in CS group when compared with control group and CS+ NaHS group (0.27±0.08 vs 0.12±0.06, 0.14±0.06, both P<0.05), there was no significant difference between CS+ PPG group and CS group. Furthermore, the IHC also showed that 3-NT significantly increased in CS group compared with control group and CS+ NaHS group (0.26±0.08 vs 0.18±0.04, 0.19±0.06, both P<0.01), there was no significant difference between CS+ PPG group and CS group as well. In addition, the small resistance pulmonary artery medial wall thickness had strong correlation with the expression level of oxidative stress marker 3-NT (r=0.906, P<0.001). Conclusion: H₂S significantly attenuates cigarette smoke induced COPD related pulmonary vascular remodeling, which could be related to its ability to decrease oxidative stress. 目的探讨硫化氢对吸烟所致慢性阻塞性肺疾病(简称慢阻肺)大鼠模型肺血管重塑的作用及机制。方法 24只清洁级雄性SD大鼠，按简单随机法分为4组：对照组、吸烟组、吸烟＋硫氢化钠(NaHS)组、吸烟＋炔丙基甘氨酸(PPG)组。对照组正常喂养，呼吸清洁空气，其余组均采用被动香烟烟雾吸入法构建慢阻肺模型，8周后对相应组的大鼠给予NaHS或PPG药物干预。16周后测定各组肺小动脉血管重塑指标；免疫组织化学方法检测各组肺血管中增殖指标增殖细胞核抗原(PCNA)以及氧化应激指标3－硝基酪氨酸(3－NT)的表达。结果吸烟组气道阻力显著高于对照组(0.859±0.283比0.578±0.088，P<0.05)，小气道病理评分明显增高，模型构建成功。吸烟组肺小动脉中膜厚度和完全肌化程度均显著高于对照组、吸烟＋NaHS组(0.54±0.20比0.37±0.12、0.39±0.08和0.61±0.16比0.20±0.12、0.34±0.13，均P<0.01)，而吸烟＋PPG组与吸烟组差异无统计学意义。吸烟组肺血管中PCNA表达均显著高于对照组、吸烟＋NaHS组(0.27±0.08比0.12±0.06、0.14±0.06，均P<0.05)，吸烟＋PPG组与吸烟组差异无统计学意义；与形态学结果相一致。吸烟组3－NT表达显著高于对照组、吸烟＋NaHS组(0.26±0.08比0.18±0.04、0.19±0.06，均P<0.01)，吸烟＋PPG组与吸烟组差异无统计学意义；且肺小动脉中膜厚度与3－NT表达水平呈强相关(r＝0.906，P<0.001)。结论硫化氢可显著改善吸烟所致慢阻肺模型的肺血管重塑，可能与其能够减轻氧化应激损伤有关。.

[Abstract] [Full Text] [Related] [New Search]