研究等業績 - その他 - 柴田　浩行

クルクミン類似体GO-Y022は心機能低下を改善した

平子 裕太, 砂川 陽一, 清水 果奈, 船本 雅文, 刀坂 泰史, 浜辺 俊英, 柴田 浩之, 小見山 麻紀, 長谷川 浩二, 森本 達也

日本薬理学会年会要旨集 ( 公益社団法人 日本薬理学会 )  96 ( 0 ) 3-B-P-214   2022年

<p><b>【Introduction】</b>We previously found that a natural p300 HAT inhibitor, curcumin (CUR), can inhibit cardiomyocyte hypertrophy and the development of heart failure <i>in vivo</i>. We focused on a CUR analog, GO-Y022, which shows stronger anti-cancer activity than CUR. The purpose of this study was to determine whether GO-Y022 inhibits p300-HAT activity and can be used as a therapeutic agent for heart failure. </p><p><b>【Methods & Results】</b><i>In vitro</i> HAT assay using recombinant p300-HAT domain showed that GO-Y022 inhibited p300-HAT activity as well as CUR. Primary cultured cardiomyocytes prepared from neonatal rats were treated with GO-Y022 or CUR and then stimulated with phenylephrine (PE) for 48 hours. One µM of GO-Y022 suppressed PE-induced histone H3K9 acetylation, hypertrophic response gene transcription, and cardiomyocyte hypertrophy to the same extent as 10 µM of CUR. C57BL/6j male mice were subjected to transverse aortic constriction (TAC) or sham operation. The TAC mice were randomly assigned to five groups: Vehicle, CUR at 1 or 50 mg/kg, or GO-Y022 at 0.2 or 1 mg/kg. After 8 weeks daily oral treatment, echocardiographic analysis showed that 1 mg/kg of GO-Y022 and 50 mg/kg of CUR improved a TAC-induced increase in left ventricular posterior wall thickness and a decrease in fractional shortening.</p><p><b>【Conclusion</b>】These results indicate that GO-Y022 strongly inhibits both PE-induced hypertrophic responses and pressure overload-induced development of heart failure. These findings suggest that GO-Y022 may be a novel candidate agent for heart failure therapy.</p>

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