| Autor: |
Araki C; Institute for Health Care Science, Suntory Wellness Limited, Kyoto 619-0284, Japan., Takemoto D; Institute for Health Care Science, Suntory Wellness Limited, Kyoto 619-0284, Japan., Kitagawa Y; Institute for Health Care Science, Suntory Wellness Limited, Kyoto 619-0284, Japan., Tateishi N; Institute for Health Care Science, Suntory Wellness Limited, Kyoto 619-0284, Japan., Rogi T; Institute for Health Care Science, Suntory Wellness Limited, Kyoto 619-0284, Japan., Izumo T; Institute for Health Care Science, Suntory Wellness Limited, Kyoto 619-0284, Japan., Kawamoto S; Departments of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan., Shibata H; Institute for Health Care Science, Suntory Wellness Limited, Kyoto 619-0284, Japan., Hara E; Departments of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan., Nakai M; Institute for Health Care Science, Suntory Wellness Limited, Kyoto 619-0284, Japan. |
| Abstrakt: |
Cellular senescence induces inflammation and is now considered one of the causes of organismal aging. Accumulating evidence indicates that age-related deterioration of mitochondrial function leads to an increase in reactive oxygen species (ROS) and DNA damage, which in turn causes cellular senescence. Thus, it is important to maintain mitochondrial function and suppress oxidative stress in order to inhibit the accumulation of senescent cells. Sesamin and its isomer episesamin are types of lignans found in sesame oil, and after being metabolized in the liver, their metabolites have been reported to exhibit antioxidant properties. However, their effects on cellular senescence remain unknown. In this study, the effects of sesamin, episesamin, and their metabolites SC1 and EC1-2 on replicative senescence were evaluated using human diploid lung fibroblasts, and TIG-3 cells. The results showed that sesamin and episesamin treatment had no effect on proliferative capacity compared to the untreated late passage group, whereas SC1 and EC1-2 treatment improved proliferative capacity and mitigated DNA damage of TIG-3 cells. Furthermore, other cellular senescence markers, such as senescence-associated secretory phenotype (SASP), mitochondria-derived ROS, and mitochondrial function (ROS/ATP ratio) were also reduced by SC1 and EC1-2 treatment. These results suggest that SC1 and EC1-2 can maintain proper mitochondrial function and suppress the induction of cellular senescence. |
