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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2007, Vol. 12 ›› Issue (4): 392-395.

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Dexamethasone suppressed over-activated endothelin system in chronic heart failure rats via anti-oxidative stress effect

NA Tao, DAI De-zai, TANG Xiao-yun, DAI Yin   

  1. Research Division of Pharmacology, China Pharmaceutical University, Nanjing 210009, Jiangsu, China
  • Received:2006-07-31 Revised:2006-07-31 Published:2020-10-30

Abstract: AIM: To investigat over-activated endothelin (ET) signaling and oxidative stress in chronic heart failure (CHF) rats and dexamethasone intervention. METHODS: Rats were performed left coronary artery ligation for 6 weeks to develop CHF and treated with dexamethasone.Masson's trichrome was used to measure myocardial fibrosis.mRNA expression of endothelin A receptor (ETA R), NF-κB and inducible nitric oxide synthase (iNOS) in myocardium were performed. RESULTS: Myocardial fibrosis was more obvious in CHF group than that in sham operation group.Dexamethasone treatment ameliorated interstitial fibrosis in myocardium of CHF rats.mRNA expression of ETAR, NF-κB and iNOS in myocardium of CHF rats was significantly upregulated compared with sham operation group, and dexamethasone down-regulated the mRNA expression of ETAR, NF-κB and iNOS. CONCLUSION: Dexamethasone inhibits over-activated ET signaling and oxidative stress in CHF myocardium through the down-regulated ETAR, which attenuate myocardial fibrosis.

Key words: dexamethasone, oxidative stress, endothelin, endothelin A receptor, NF-κB, nitricoxide synthase, chronic heart failure

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