Identification of Cellular Isoschaftoside-Mediated Anti-Senescence Mechanism in RAC2 and LINC00294

Author:

Lee Yun Haeng1,So Byeong Hyeon1,Lee Kyeong Seon2,Kuk Myeong Uk1,Park Ji Ho1,Yoon Jee Hee1,Lee Yoo Jin1,Kim Du Yeol1,Kim Min Seon1,Kwon Hyung Wook13ORCID,Byun Youngjoo2ORCID,Lee Ki Yong2ORCID,Park Joon Tae13ORCID

Affiliation:

1. Division of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea

2. College of Pharmacy, Korea University, Sejong 30019, Republic of Korea

3. Convergence Research Center for Insect Vectors, Incheon National University, Incheon 22012, Republic of Korea

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.

Funder

Korea Health Technology R&D Project through the Korea Health Industry Development Institute

Ministry of Health & Welfare

Priority Research Centers Program

National Research Foundation of Korea (NRF) funded by the Ministry of Education and NRF of Korea grants funded by the Korean Government

Publisher

MDPI AG

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