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目的:探讨硫化氢(H2S)在吸烟(CS)联合脂多糖(LPS)建立的大鼠慢性阻塞性肺疾病(COPD)模型中的抗氧化作用。方法:32只清洁级健康雄性SD(Sprague-Dawley)大鼠,随机分为4组:对照组(control)、CS+LPS组、CS+LPS+硫氢化钠(NaHS,H2S供体)组、CS+LPS+炔丙基甘氨酸(PPG,胱硫醚-γ-裂解酶抑制剂)组。30 d后测定大鼠肺功能,光镜观察肺组织病理变化并予评分;测定血浆中H2S含量及肺组织中胱硫醚-γ-裂解酶(CSE)蛋白表达;检测肺组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)及过氧化氢酶(CAT)活性以反映氧化应激。结果:与对照组相比,CS+LPS组大鼠呼气峰流速(PEF)下降24%(P<0.01),气道内压(IP)升高66%(P<0.01),肺组织病理评分升高(P<0.01);NaHS或PPG干预后,与CS+LPS组比较,肺功能无改变;NaHS干预后,病理评分下降(P<0.05)。在第16 d时,CS+LPS组血浆中H2S含量较对照组升高26%(P<0.05);30 d后,CS+LPS+PPG组较CS+LPS组H2S含量降低22%(P<0.01)。CS+LPS组中CSE蛋白表达较对照组升高(P<0.01);与CS+LPS组比较,CS+LPS+NaHS组和CS+LPS+PPG组无显著差异。与对照组相比,CS+LPS组肺组织中MDA含量升高24%(P<0.05),总SOD活性升高47%(P<0.01),CAT活性升高52%(P<0.01);与CS+LPS组相比,NaHS干预后,MDA含量降低21%(P<0.05),总SOD活性及CAT活性无显著差异;而PPG干预后,总SOD活性下降33%(P<0.05)。结论:H2S在COPD大鼠中起到抗氧化作用,CSE/H2S途径可能参与COPD疾病的发展。
AIM: To investigate the anti-oxidative effects of hydrogen sulfide (H2S) in a rat model of chronic obstructive pulmonary disease (COPD) established by smoking (CS) combined with lipopolysaccharide (LPS). Methods: Thirty-two healthy male Sprague-Dawley rats were randomly divided into 4 groups: control group, CS + LPS group, CS + LPS + sodium hydrosulfide (NaHS) donor group + LPS + propargylglycine (PPG, cystathionine-γ-lyase inhibitor) group. The lung function of rats was measured after 30 days. The pathological changes of lung tissue were observed under light microscope and scored. The content of H2S in plasma and the expression of cystathionine-γ-lyase (CSE) in lung tissue were measured. (MDA) content, superoxide dismutase (SOD) and catalase (CAT) activity to reflect oxidative stress. Results: Compared with the control group, the expiratory peak flow velocity (PEF) decreased by 24% (P <0.01) and the airway pressure (IP) increased by 66% (P <0.01) (P <0.01). After NaHS or PPG intervention, lung function did not change compared with CS + LPS group. Pathological score decreased after NaHS intervention (P <0.05). On the 16th day, the content of H2S in the plasma of CS + LPS group increased by 26% compared with the control group (P <0.05). After 30 days, the content of H2S in CS + LPS + PPG group decreased by 22% 0.01). CSE protein expression in CS + LPS group was higher than that in control group (P <0.01). Compared with CS + LPS group, there was no significant difference between CS + LPS + NaHS group and CS + LPS + PPG group. Compared with the control group, the content of MDA in the lung tissue of CS + LPS group increased by 24% (P <0.05), the total SOD activity increased by 47% (P <0.01) and the CAT activity increased by 52% (P <0.01). Compared with the CS + LPS group, the content of MDA decreased 21% (P <0.05) and the total SOD activity and CAT activity had no significant difference when compared with CS + LPS group, while the total SOD activity decreased 33% (P <0.05) after PPG intervention. Conclusions: H2S plays an antioxidant role in COPD rats. CSE / H2S pathway may be involved in the development of COPD.