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Voluntary exercise reverses immune aging induced by oxidative stress in aging mice
- Voluntary exercise reverses immune aging induced by oxidative stress in aging mice
- Lee, Ji-Young; Paik, Il-Young; Kim, Joo Young
- Ewha Authors
- SCOPUS Author ID
- Issue Date
- Journal Title
- EXPERIMENTAL GERONTOLOGY
- EXPERIMENTAL GERONTOLOGY vol. 115, pp. 148 - 154
- Aging; Immunosenescence; Oxidative stress; Vitamin E; Voluntary exercise
- PERGAMON-ELSEVIER SCIENCE LTD
- SCI; SCIE; SCOPUS
- Document Type
- Excessive oxidative stress leads to aging due to persistent damage to the cells, tissues, and the entire organism. Immunosenescence is also a devastating consequence of oxidative stress, but there is a lack of research on effective ways to overcome it. In this study, we used physiologic and immunological aging mouse models that had sustained oxidative stress to investigate whether voluntary exercise and/or antioxidant treatment could overcome oxidative damage as well as aging. We established an aging model induced by continuously administering D-galactose (D-gal) to 6-week-old female C57BL/6J mice. We also assessed reversal of immunosenescence by providing free-wheel running and vitamin E (vit E) supplementation to this aging model. As an aging index, the level of advanced glycation end products (AGEs) in the blood was measured. Phenotypes of T cells in the thymus and spleen were examined as an index of immunosenescence. Intracellular reactive oxygen species (ROS) levels in the mouse spleen and levels of AGEs in the blood were significantly higher after 6 weeks of D-gal administration. In addition, immunosenescence was observed, in which the naive:effector cell ratio in the spleen decreased. After 4 weeks of free-wheel running and vit E administration, both intracellular ROS and serum AGE levels decreased. Above all, free-wheel running restored the naive:effector ratio of cytotoxic T lymphocytes reduced by D-gal administration. Taken together, these results suggest that voluntary exercise may be effective in restoring immunosenescence induced by oxidative stress.
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