[Expression of Rock2 and TGF-ß1 mRNA and glucocorticoid intervention in asthmatic rats].

OBJECTIVE: To study the roles of rhoassociated coiled coil forming protein kinase 2 (Rock2) and transforming growth factor-ß1 (TGF-ß1) mRNA in acute asthma and the effect of glucocorticoid intervention on the Rock2 and TGF-ß1 mRNA expression in rats. METHODS: Forty-eight male rats were randomly divided into 4 groups (n=12 each): asthma, control, dexamethasone treated (DXM) and budesonide treated (BUD). Rat model of asthma was prepared by the ovalbumin (OVA) challenge. The animals were sacrificed 24 hrs after the last challenge. The total cell number and differentiation cell number were counted in bronchoalveolar lavage fluid (BALF). The protein expression of Rock2 was ascertained by immunohistochemistry and the mRNA expression of TGF-ß1 was ascertained by hybridization in situ. RESULTS: The pathological changes in the BUD and the DXM groups were alleviated when compared with the asthma group. The total cell number and the percentage of eosinophil (EOS), polymorphonuclear leukocytes (PMN) and lymphocytes (Lym) in BALF in the asthma group were significantly higher than those in the control group (P<0.01). The percentage of macrophage (Mф) in the asthma group was significantly lower than that in the control group (P<0.01). The total cell number and the percentage of EOS and Lym in BALF in the DXM and the BUD groups decreased, while the percentage of Mф increased significantly compared with those in the asthma group (P<0.01). The Rock2 and TGF-ß1 mRNA expression in lung tissues in the asthma group increased significantly compared with those in the control, BUD and DXM groups, while there were no significant differences in the Rock2 expression and TGF-ß1 mRNA expression between the DXM or BUD group and the control group. CONCLUSIONS: The expression of Rock2 and TGF-ß1 mRNA in lung tissues is increased in rats with acute asthma. Glucocorticoids can significantly decrease the expression of Rock2 and TGF-ß1 in lung tissues, thus alleviates airway inflammation.

[Regulative mechanism of budesonide on endogenous hydrogen sulfide, cystathionine-gamma-lyase and cystathionine-beta-synthase system in asthmatic rats].

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.