title: [Regulative mechanism of budesonide on endogenous hydrogen sulfide, cystathionine-gamma-lyase and cystathionine-beta-synthase system in asthmatic rats].
abstract: 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.
authors: Department of Pediatrics, Taizhou Hospital, Linhai, Zhejiang 317000, China. lishaobo71@yahoo.com.cn
authors: Shao-Bo
authors: SB
authors: Li
authors: Xia-Sheng
authors: XS
authors: Tong
authors: Xin-Xin
authors: XX
authors: Wang
authors: Xiao-Hong
authors: XH
authors: Jin
authors: Hui
authors: H
authors: Ye
mesh_terms: D000818:Animals; D001249:Asthma / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D019819:Budesonide / Q000494:pharmacology*; D003541:Cystathionine beta-Synthase / Q000235:genetics / Q000502:physiology*; D003542:Cystathionine gamma-Lyase / Q000235:genetics / Q000502:physiology*; D006862:Hydrogen Sulfide / Q000378:metabolism*; D008297:Male; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D012333:RNA, Messenger; D019819:Budesonide; D003541:Cystathionine beta-Synthase; D003542:Cystathionine gamma-Lyase; D006862:Hydrogen Sulfide