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PS23通过确保SAMP8小鼠的线粒体功能来减缓与年龄相关的肌肉流失。

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

作者信息

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

机构信息

Department of Food Science, Nutrition, and Nutraceutical Biotechnology, Shih Chien University, Taipei, Taiwan.

Graduate Institute of Metabolism and Obesity Sciences, Taipei Medical University, Taipei, Taiwan.

出版信息

Aging (Albany NY). 2019 Jan 29;11(2):756-770. doi: 10.18632/aging.101782.

DOI:10.18632/aging.101782
PMID:30696799
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6366975/
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. 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.

摘要

肌肉减少症是老年人群中常见的一种机能损害,会导致晚年出现不良后果;它可能由与年龄相关的变化引起。据报道,只有少数几种策略可减少肌肉减少症。PS23(LPPS23)已被报道可延缓一些与年龄相关的疾病。因此,我们在此研究LPPS23是否能减缓与年龄相关的肌肉流失及其潜在机制。将雌性衰老加速小鼠易感8型(SAMP8)小鼠分为三组(每组n = 6):未衰老组(16周龄)、对照组(28周龄)和PS23组(28周龄)。对照组和PS23组分别给予生理盐水和LPPS23。我们通过分析体重和组成、肌肉力量、蛋白质摄取、线粒体功能、活性氧(ROS)、抗氧化酶和炎症相关细胞因子来评估LPPS23的作用。LPPS23显著减轻了与年龄相关的肌肉质量和力量下降。与对照组相比,未衰老组和PS23组表现出更高的线粒体功能、白细胞介素10、抗氧化酶和蛋白质摄取。此外,未衰老组和PS23组的炎症细胞因子和ROS低于对照组。综上所述,LPPS23减缓了衰老过程中肌肉减少症的进展;这种作用可能是通过减少与年龄相关的炎症和ROS来维持线粒体功能,并通过保持SAMP8小鼠的蛋白质摄取来实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/63fc922732f2/aging-11-101782-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/94b73c3cb6b1/aging-11-101782-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/00377b7b972c/aging-11-101782-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/00b4362fde07/aging-11-101782-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/d03674bc1830/aging-11-101782-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/88eaa1813a24/aging-11-101782-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/63fc922732f2/aging-11-101782-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/94b73c3cb6b1/aging-11-101782-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/00377b7b972c/aging-11-101782-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/00b4362fde07/aging-11-101782-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/d03674bc1830/aging-11-101782-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/88eaa1813a24/aging-11-101782-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d55d/6366975/63fc922732f2/aging-11-101782-g006.jpg

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