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Research Paper|Volume 11, Issue 2|pp 756—770

Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice

Li-Han Chen1, Shih-Yi Huang2, Kuo-Chin Huang3,4,5, Chih-Chieh Hsu6, Kuen-Cheh Yang5, Lin-Ai Li1, Ching-Hung Chan1, Hui-Yu Huang1,2
  • 1Department of Food Science, Nutrition, and Nutraceutical Biotechnology, Shih Chien University, Taipei, Taiwan
  • 2Graduate Institute of Metabolism and Obesity Sciences, Taipei Medical University, Taipei, Taiwan
  • 3Department of Family Medicine, School of Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan
  • 4Department of Family Medicine, National Taiwan University Hospital, Taipei, Taiwan
  • 5Department of Family Medicine, National Taiwan University Hospital Beihu Branch, Taipei, Taiwan
  • 6Research and Development Department, Bened Biomedical Co., Ltd., Taipei, Taiwan
  • 7Health Science and Wellness Center, National Taiwan University, Taipei, Taiwan

* * Equal contribution

Received: September 17, 2018Accepted: January 15, 2019Published: January 29, 2019
https://doi.org/10.18632/aging.101782

Copyright: © 2019 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Sarcopenia is a common impairment in the elderly population responsible for poor outcomes later in life; it can be caused by age-related alternations. Only a few strategies have been reported to reduce sarcopenia. Lactobacillus paracasei PS23 (LPPS23) has been reported to delay some age-related disorders. Therefore, here we investigated whether LPPS23 decelerates age-related muscle loss and its underlying mechanism. Female senescence-accelerated mouse prone-8 (SAMP8) mice were divided into three groups (n=6 each): non-aging (16-week-old), control (28-week-old), and PS23 (28-week-old) groups. The control and PS23 groups were given saline and LPPS23, respectively. We evaluated the effects of LPPS23 by analyzing body weight and composition, muscle strength, protein uptake, mitochondrial function, reactive oxygen species (ROS), antioxidant enzymes, and inflammation-related cytokines. LPPS23 significantly attenuated age-related decreases of muscle mass and strength. Compared to the control group, the non-aging and PS23 groups exhibited higher mitochondrial function, IL10, antioxidant enzymes, and protein uptake. Moreover, inflammatory cytokines and ROS were lower in the non-aging and PS23 groups than the control group. Taken together, LPPS23 extenuated sarcopenia progression during aging; this effect might have been enacted by preserving the mitochondrial function via reducing age-related inflammation and ROS and by retaining protein uptake in the SAMP8 mice.