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Endocrine Abstracts (2016) 41 EP756 | DOI: 10.1530/endoabs.41.EP756


Pharmacological effects of urocortin (Ucn) on nicotine-induced oxidative stress to cardiomyocytes

Keiichi Ikeda1,3, Yoshinobu Manome1 & Katsuyoshi Tojo2,3


1Division of Molecular Cell Biology, Core Research Facilities for Basic Science, Research Center for Medical Sciences, The Jikei University School of Medicine, Tokyo, Japan; 2Department of Internal Medicine, Division of Diabetes and Endocrinology, The Jikei University School of Medicine, Tokyo, Japan; 3Institute of Clinical Medicine and Research, The Jikei University School of Medicine, Kashiwa City, Chiba Prefecture, Japan.

Based on the known oxidative stress of nicotine, we examined the effects of Ucn I on nicotine-induced oxidative stress in HL-1 cardiomyocytes. HL-1 cardiomyocytes is plated on 96-well plate at a density of 2.0×104 cells/well with Claycomb medium containing 10% fetal bovine serum (FBS) and 0.1 mmol/L epinephrine. After starvation of FBS and epinephrine with Claycomb medium, cells were stimulated with or without (+/−)-nicotine, Ucn I and Ucn II. Cells were also stimulated with (+/−)-nicotine after knocking down of Ucn I mRNA. Oxidative stress is evaluated by conversion of 2′, 7′-dichlorodihydrofluorescin diacetate to 2′, 7′-dichlorodihydrofluorescein. (+/−)-nicotine exereted significant oxidative stress on HL-1 cardiomyocytes, while (−)-nicotine, a cis-trans isomer of (+/−)-nicotine, did not exert significant oxidative actions on HL-1 cardiomyocytes. Ucn I suppressed not only (+/−)-nicotine-induced oxidative stress, but also oxidative stress in standard culture condition in HL-1ardiomyocytes. In addition, knockdown of Ucn I by siRNA enhanced (+/−)-nicotine-induced oxidative stress. On the contrary, Ucn II alone, another agonist of corticotropin-releasing factor type 2 receptor, did not exert significant anti-oxidative stress action at the basal condition, but reduced (+/−)-nicotine-induced oxidative stress. The present results indicate that Ucn I may exert anti-oxidative actions on cardiomyocytes, of which mechanism of actions are still remained to be clarified.

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