Identification of Cellular Isoschaftoside-Mediated Anti-Senescence Mechanism in RAC2 and LINC00294
Authors:
- Yun Haeng LeeYLYun Haeng Lee
- Byeong Hyeon SoBSByeong Hyeon So
- Kyeong Seon LeeKLKyeong Seon Lee
- Myeong Uk KukMKMyeong Uk Kuk
- Ji Ho ParkJPJi Ho Park
- Jee Hee YoonJYJee Hee Yoon
- Yoo Jin LeeYLYoo Jin Lee
- Du Yeol KimDKDu Yeol Kim
- Min Seon KimMKMin Seon Kim
- Hyung Wook KwonHKHyung Wook Kwon
- Youngjoo ByunYBYoungjoo Byun
- Ki Yong LeeKLKi Yong Lee
Open Access
- 4 September 2024
- Vol. 29 (17) , 4182
Abstract
As cellular senescence, reactive oxygen species (ROS) accumulate excessively, causing cellular damage. Flavonoids derived from natural products are known for their antioxidant effects and their ability to delay cellular senescence. Previous studies have attempted to mitigate cellular senescence using flavonoids from natural sources. However, the detailed mechanisms and regulatory targets of some flavonoids exhibiting antioxidant effects have not been fully elucidated. Therefore, we screened a library of flavonoids for antioxidant properties. Isoschaftoside, a glycosidic flavonoid, significantly reduced ROS levels in senescent cells. It was found that mitochondrial function was restored, and dependence on glycolysis was reduced in senescent cells treated with isoschaftoside. Additionally, we identified that isoschaftoside suppresses ROS by reducing the expression of RAC2 and LINC00294 in senescent cells. Taken together, this study establishes a novel mechanism for ROS inhibition and the regulation of cellular senescence by isoschaftoside. Our findings contribute important insights to antioxidant and anti-senescence research.Keywords
Funding Information
- Ministry of Health & Welfare, Republic of Korea (HP23C0024)
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