布地奈德对哮喘大鼠内源性硫化氢、胱硫醚-γ-裂解酶和胱硫醚-β-合酶系统的调节机制

Li Shao-Bo, Tong Xia-Sheng, Wang Xin-Xin, Jin Xiao-Hong, Ye Hui

Department of Pediatrics, Taizhou Hospital, Linhai, Zhejiang 317000, China.

Zhongguo Dang Dai Er Ke Za Zhi. 2010 Aug;12(8):654-7.

OBJECTIVE

To investigate plasma hydrogen sulfide (H₂S) levels and cystathionine-gamma- lyase (CSE) and cystathionine-beta-synthase (CBS) mRNA expression in the lung tissues in asthmatic rats and to explore the roles of endogenous H₂S, CSE and CBS system in the pathogenesis of asthma.

METHODS

Thirty male Sprague-Dawley rats (age 5 to 7 weeks) were randomly divided into three groups: control, asthma and budesonide treatment (n = 10 each). The asthma model was established by ovalbumin (OVA) sensitization and challenge. The budesonide treatment group received inhaled budesonide before challenge. The contents of plasma H₂S were measured by spectrophotometry. The levels of CSE and CBS mRNA in the lung tissues were examined by reverse transcriptase polymerase chain reaction (RT-PCR).

RESULTS

The contents of plasma H₂S in the asthma group (61 ± 16 μmol/L) were significantly lower than those in the control group (84 ± 15 μmol/L) (P<0.01). The contents of plasma H₂S in the budesonide treatment group (71 ± 14 μmol/L) were not statistically different from those in the control and asthma groups. CSE mRNA and CBE mRNA expression in the asthma group were significantly lower than those in the control group (P < 0.01). The budesonide treatment group had a decreased CSE mRNA expression and CBE mRNA expression compared with the control group, but had significantly increased CSE and CBE mRNA expression compared with the asthma group (P < 0.01). There was a significantly negative correlation between H₂S contents in plasma and total inflammatory cells in bronchoalveolar lavage fluid (n = 30, r = -0.549, P < 0.01).

CONCLUSIONS

Plasma H₂S levels and CSE and CBS expression in the lung decrease in asthmatic rats, which possibly promotes inflammatory cell aggregation to the airway. Budesonide may alleviate airway inflammation in asthmatic rats possibly through the system of endogenous H₂S, CSE and CBS.

目的

探讨哮喘大鼠血浆硫化氢（H₂S）水平及肺组织中胱硫醚-γ-裂解酶（CSE）和胱硫醚-β-合酶（CBS）mRNA的表达，以探究内源性H₂S、CSE和CBS系统在哮喘发病机制中的作用。

方法

将30只雄性Sprague-Dawley大鼠（5至7周龄）随机分为三组：对照组、哮喘组和布地奈德治疗组（每组10只）。通过卵清蛋白（OVA）致敏和激发建立哮喘模型。布地奈德治疗组在激发前吸入布地奈德。采用分光光度法测定血浆H₂S含量。通过逆转录聚合酶链反应（RT-PCR）检测肺组织中CSE和CBS mRNA的水平。

结果

哮喘组血浆H₂S含量（61±16μmol/L）显著低于对照组（84±15μmol/L）（P<0.01）。布地奈德治疗组血浆H₂S含量（71±14μmol/L）与对照组和哮喘组相比无统计学差异。哮喘组CSE mRNA和CBE mRNA表达显著低于对照组（P<0.01）。与对照组相比，布地奈德治疗组CSE mRNA表达和CBE mRNA表达降低，但与哮喘组相比，CSE和CBE mRNA表达显著增加（P<0.01）。血浆H₂S含量与支气管肺泡灌洗液中总炎性细胞之间存在显著负相关（n = 30，r = -0.549，P<0.01）。