Effects of endogenous sulfur dioxide on monocrotaline-induced pulmonary hypertension in rats
Effects of endogenous sulfur dioxide on monocrotaline-induced pulmonary hypertension in rats
复制标题
内源性二氧化硫对野百合碱所致大鼠肺动脉高压的影响
DOI：
10.1111/j.1745-7254.2008.00864.x
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发表时间：
2008-10-01
影响因子：
8.2
通讯作者：
Du, Jun-bao
中科院分区：
文献类型：
--
作者：
Jin, Hong-fang;Du, Shu-xu;Du, Jun-bao
目的：探讨内源性二氧化硫（SO2）对野百合碱（MCT）诱导的大鼠肺动脉高压（PH）的保护作用。方法：40只Wistar大鼠随机分为MCT组、MCT+ L-天冬氨酸-β-异羟肟酸（HDX）组、MCT+SO2组和对照组。评估平均肺动脉压（mPAP）和肺动脉结构变化。测定SO2含量、天冬氨酸转氨酶活性和基因表达。结果：与对照组相比，MCT组大鼠mPAP和右心室/（左心室+室间隔）显著升高（P<0.01），肺血管结构发生重构，肺组织匀浆SOD、GSH-Px、CAT、GSH和MDA水平显著升高（P <0.01），SO2含量、天冬氨酸氨基转移酶活性和基因表达显著升高。MCT+ HDX治疗组大鼠肺组织和血浆SO2含量及天门冬氨酸氨基转移酶活性明显降低，mPAP和肺血管结构重建明显加重，肺组织匀浆中SOD、CAT和GSH含量明显降低（P<0.01）。结论：内源性SO2可能在MCT诱导的肺动脉高压的发病机制中起保护作用，并促进内源性抗氧化能力的增强。
AbstractAim:The present study aimed to explore the protective effect of endogenous sulfur dioxide (SO2) in the development of monocrotaline (MCT)-induced pulmonary hypertension (PH) in rats.Methods:Forty Wistar rats were randomly divided into the MCT group receiving MCT treatment, the MCT+L-aspartate-β-hydroxamate (HDX) group receiving MCT plus HDX treatment, the MCT+SO2 group receiving MCT plus SO2 donor treatment, and the control group. Mean pulmonary artery pressure (mPAP) and structural changes in pulmonary arteries were evaluated. SO2 content, aspartate aminotransferase activity, and gene expression were measured. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), reduced glutathione (GSH), oxidized glutathione, and malondialdehyde (MDA) levels were assayed.Results:In the MCT-treated rats, mPAP and right ventricle/(left ventricle+septum) increased significantly (P<0.01), pulmonary vascular structural remodeling developed, and SOD, GSH-Px, CAT, GSH, and MDA levels of lung homogenates significantly increased (P<0.01) in association with the elevated SO2 content, aspartate aminotransferase activity, and gene expression, compared with the control rats. In the MCT+HDX-treated rats, lung tissues and plasma SO2 content and aspartate aminotransferase activities decreased significantly, whereas the mPAP and pulmonary vascular structural remodeling were markedly aggravated with the decreased SOD, CAT, and GSH levels of lung tissue homogenates compared with the MCT-treated rats (P<0.01). In contrast, with the use of a SO2 donor, the pulmonary vascular structural remodeling was obviously lessened with elevated lung tissue SOD, GSH-Px, and MDA content, and plasma SOD, GSH-Px, and CAT levels.Conclusion:Endogenous SO2 might play a protective role in the pathogenesis of MCT-induced PH and promote endogenous antioxidative capacities.