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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 60:1252-1264 (2005)
© 2005 The Gerontological Society of America

Betaine Suppresses Proinflammatory Signaling During Aging: The Involvement of Nuclear Factor-{kappa}B via Nuclear Factor-Inducing Kinase/I{kappa}B Kinase and Mitogen-Activated Protein Kinases

Eun Kyung Go1, Kyung Jin Jung1, Ji Young Kim1, Byung Pal Yu2,3 and Hae Young Chung1,2,

1 Department of Pharmacy, College of Pharmacy, and 2Longevity Life Science and Technology Institutes Pusan National University, Gumjung-ku, Busan, Republic of Korea.
3 Department of Physiology, The University of Texas Health Science Center at San Antonio.

Address correspondence to Hae-Young Chung, PhD, Department of Pharmacy, College of Pharmacy, Pusan National University, San 30, Jang-jun-dong, Gumjung-ku, Busan, 609-735, Korea. E-mail: hyjung{at}pusan.ac.kr

Betaine is an important human nutrient obtained from various foods. In the present study, we assessed the anti-inflammatory effect of betaine on nuclear factor-{kappa}B (NF-{kappa}B) during aging. Sprague-Dawley (SD) rats, ages 7 and 21 months, were used in this study. The older rats were fed betaine. To elucidate the effect of betaine on oxidative stress-induced NF-{kappa}B and its signaling pathway at molecular levels, YPEN-1 cells were used. Results showed that betaine suppressed NF-{kappa}B and its related gene expressions of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), vascular cell adhesion molecule-1 (VCAM-1), and intracellular cell adhesion molecule-1 (ICAM-1) in aged kidney. Furthermore, betaine attenuated oxidative stress-induced NF-{kappa}B via nuclear factor-inducing kinase/I{kappa}B kinase (NIK/IKK) and mitogen-activated protein kinases (MAPKs) in the YPEN-1 cells. On the basis of these results, we concluded that betaine suppressed the age-related NF-{kappa}B activities associated with upregulated NIK/IKK and MAPKs that were induced by oxidative stress. Thus, betaine might be useful as a preventive agent against the activation of NF-{kappa}B induced during inflammation and aging.




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Copyright © 2005 by The Gerontological Society of America.