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[Effects of H2 relaxin on the expression of Epac in a murine model of chronic asthma].

AbstractOBJECTIVE:
To explore the effects of H(2) relaxin on the expression of exchange protein directly activated by cyclic adenosine monophosphate (Epac) in a murine model of chronic asthma and the roles in the management of airway remodelling.
METHODS:
Thirty-two BALB/c mice were randomly divided into 4 groups of normal control, asthma, vehicle control and relaxin treatment (n = 8 each). They were sensitized and challenged with ovalbumin to establish a chronic asthmatic model. The vehicle control and relaxin treatment groups were subcutaneously injected with saline and relaxin (0.25 mg×kg(-1)×d(-1)) respectively. Alteration of airway inflammation was observed by hematoxylin-eosin (HE) staining. The airway expressions of proliferating cell nuclear antigen (PCNA) and α-smooth muscle actin (α-SMA) were evaluated by immunohistochemistry. The protein expression of Epac and phosphorylated extracellular signal regulated kinases1/2 (p-ERK1/2) were detected by Western blot.
RESULTS:
Compared to those in the normal control group, massive infiltration of inflammatory cells, airway stenosis, bronchial smooth muscle hypertrophy were present in the asthmatic and vehicle control groups. The above-mentioned changes were significantly ameliorated in the relaxin treatment group. The percentage of PCNA positive cells (34.8% ± 6.1%, 33.5% ± 6.6%) and the expression of α-SMA ((1.70 ± 0.25), (1.54 ± 0.24) µm(2)/µm) in the asthmatic and vehicle control groups were significantly higher than those in the normal control group (9.9% ± 2.6%, (0.51 ± 0.16) µm(2)/µm) (all P < 0.05) while administration of relaxin decreased the airway expression levels of PCNA and α-SMA (22.9% ± 5.2%, (1.06 ± 0.25) µm(2)/µm) (all P < 0.05). The results of Western blot showed that the expression levels of Epac in the asthmatic and vehicle groups (0.62 ± 0.12, 0.68 ± 0.11) were lower than those in the control group (1.50 ± 0.17) (all P < 0.05) while it significantly increased in the relaxin group (1.08 ± 0.15) (all P < 0.05). The levels of phosphorylation of ERK1/2 in the asthmatic and vehicle groups (1.45 ± 0.13, 1.36 ± 0.09) were higher than those in the control group (0.38 ± 0.17) (all P < 0.05) while it decreased in the relaxin treatment group (0.72 ± 0.06) (all P < 0.05). No differences existed in all parameters between the asthmatic and vehicle groups (P > 0.05).
CONCLUSION:
Relaxin alleviates the airway inflammation and airway smooth muscle cell proliferation in a murine model of chronic asthma probably through activating Epac and inhibiting the phosphorylation of ERK1/2.
AuthorsShu-guang Han, Hong-qing Zhao, Lei Lü, Xin-hua Wang, Xun Wang
JournalZhonghua yi xue za zhi (Zhonghua Yi Xue Za Zhi) Vol. 92 Issue 46 Pg. 3305-9 (Dec 11 2012) ISSN: 0376-2491 [Print] China
PMID23328520 (Publication Type: English Abstract, Journal Article)
Chemical References
  • Actins
  • Epac protein, mouse
  • Guanine Nucleotide Exchange Factors
  • Proliferating Cell Nuclear Antigen
  • alpha-smooth muscle actin, mouse
  • Relaxin
Topics
  • Actins (metabolism)
  • Airway Remodeling
  • Animals
  • Asthma (metabolism)
  • Female
  • Guanine Nucleotide Exchange Factors (metabolism)
  • Lung (drug effects, metabolism)
  • MAP Kinase Signaling System
  • Mice
  • Mice, Inbred BALB C
  • Oxidative Phosphorylation
  • Proliferating Cell Nuclear Antigen (metabolism)
  • Relaxin (pharmacology)

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