Korean J Physiol Pharmacol.  2021 Jul;25(4):297-305. 10.4196/kjpp.2021.25.4.297.

Luteolin inhibits H2O2 -induced cellular senescence via modulation of SIRT1 and p53

Affiliations
  • 1Department of Biochemistry, Wonkwang University School of Medicine, Iksan 54538, Korea

Abstract

Luteolin, a sort of flavonoid, has been reported to be involved in neuroprotective function via suppression of neuroinflammation. In this study, we investigated the protective effect of luteolin against oxidative stress-induced cellular senescence and its molecular mechanism using hydrogen peroxide (H2O2)-induced cellular senescence model in House Ear Institute-Organ of Corti 1 cells (HEI-OC1). Our results showed that luteolin attenuated senescent phenotypes including alterations of morphology, cell proliferation, senescence-associated β-galactosidase expression, DNA damage, as well as related molecules expression such as p53 and p21 in the oxidant challenged model. Interestingly, we found that luteolin induces expression of sirtuin 1 in dose- and time-dependent manners and it has protective role against H2O2 -induced cellular senescence by upregulation of sirtuin 1 (SIRT1). In contrast, the inhibitory effect of luteolin on cellular senescence under oxidative stress was abolished by silencing of SIRT1. This study indicates that luteolin effectively protects against oxidative stress-induced cellular senescence through p53 and SIRT1. These results suggest that luteolin possesses therapeutic potentials against age-related hearing loss that are induced by oxidative stress.

Keyword

Cellular senescence; Hydrogen peroxide; Luteolin; Sirtuin 1; Tumor suppressor protein p53
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