Article Publish Status: FREE
Abstract Title:

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

Abstract Source:

Aging (Albany NY). 2019 Jan 29 ;11(2):756-770. PMID: 30696799

Abstract Author(s):

Li-Han Chen, Shih-Yi Huang, Kuo-Chin Huang, Chih-Chieh Hsu, Kuen-Cheh Yang, Lin-Ai Li, Ching-Hung Chan, Hui-Yu Huang

Article Affiliation:

Li-Han Chen


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.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.

Study Type : Animal Study

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