Luteolin inhibits H2O2 -induced cellular senescence via modulation of SIRT1 and p53
10.4196/kjpp.2021.25.4.297
- Author:
Ri Zhe ZHU
1
;
Bing Si LI
;
Shang Shang GAO
;
Jae Ho SEO
;
Byung-Min CHOI
Author Information
1. Department of Biochemistry, Wonkwang University School of Medicine, Iksan 54538, Korea
- Publication Type:Original Article
- From:The Korean Journal of Physiology and Pharmacology
2021;25(4):297-305
- CountryRepublic of Korea
- Language:English
-
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.
