Endocrine Abstracts

Cardioprotective actions of urocortin (Ucn) I have been proposed by several studies and may play a critical role on stress adaptation. And one of the beneficial actions on cardiovascular cells may be anti-oxidative actions. In addition, Ucn I may be regulated by oxidative stress, therefore, the present study is designed to reveal anti-oxidative actions of Ucns on cardiomyocytes. Mouse atrial cell line, HL-1 cardiomyocytes, was cultured in standard Claycomb medium supplemented with 10% fetal bovine serum and norepinephrine. Thereafter, HL-1 cardiomyocytes were further incubated in serum- and norepinephrine-free Claycomb medium containing 0.1% BSA with or without Ucn I, Ucn II, and astressin 2B, an antagonist of corticotroipin-releasing factor type 2 receptors (CRFR2) and oxidative stress was evaluated by measurement of conversion of 2′,7′-dichlorodihydrofluorescin diacetate to 2′,7′-dichlorodihydrofluorescein. Interestingly, Ucn I, but not Ucn II, suppressed oxidative stress of HL-1 cardiomyocytes without other stimulatory agents of oxidative stress. In addition, astressin 2B (10–6 mol/l) did not abolish the anti-oxidative action of Ucn I. It have been already reported that Ucn I exert anti-oxidative actions against angiotensin II-induced oxidative stress in human umbilical vein endothelial cells. Taken together with the present results, Ucn I may also exert cardioprotective actions via the anti-oxidative stress in cardiomyocytes, not via the CRFR2 signaling pathway.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.