Identification of Cellular Isoschaftoside-Mediated Anti-Senescence Mechanism in RAC2 and LINC00294
Yun Haeng Lee1, Byeong Hyeon So1, Kyeong Seon Lee2
1Division of Life Sciences, College of Life Sciences and Bioengineering, 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.
Insights
Isoschaftoside, a natural flavonoid, reduces damaging reactive oxygen species (ROS) in aging cells. This antioxidant compound restores mitochondrial function and lowers glycolysis dependence, offering new insights into anti-senescence strategies.
Area of Science:
- Biochemistry
- Cell Biology
- Gerontology
Background:
- Cellular senescence is characterized by excessive reactive oxygen species (ROS) accumulation, leading to cellular damage.
- Flavonoids, natural compounds, possess antioxidant properties and can delay cellular senescence.
- The precise mechanisms and regulatory targets of some antioxidant flavonoids remain incompletely understood.
Purpose of the Study:
- To screen a library of flavonoids for antioxidant properties.
- To investigate the effects of isoschaftoside on ROS levels and cellular senescence.
- To elucidate the underlying molecular mechanisms of isoschaftoside's action.
Main Methods:
- Screening of a flavonoid library for antioxidant activity.
- Treatment of senescent cells with isoschaftoside.
- Assessment of ROS levels, mitochondrial function, and glycolysis dependence.
- Analysis of gene expression changes (RAC2 and LINC00294).
Main Results:
- Isoschaftoside significantly reduced ROS levels in senescent cells.
- Mitochondrial function was restored, and glycolysis dependence decreased upon isoschaftoside treatment.
- Isoschaftoside suppressed ROS by downregulating the expression of RAC2 and LINC00294.
Conclusions:
- Isoschaftoside exhibits significant antioxidant and anti-senescence properties.
- A novel mechanism involving the reduction of RAC2 and LINC00294 expression underlies isoschaftoside's ROS inhibition.
- This study provides valuable insights into antioxidant and anti-senescence research through the action of isoschaftoside.
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