期刊
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
卷 75, 期 11, 页码 2081-2088出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/glaa214
关键词
Apigenin; Apoptosis; Mitophagy; Reactive oxygen species; Skeletal muscle atrophy
资金
- National Natural Science Foundation of China [81874394, 81673814]
- Science and Technology Planning Project of Shenzhen Municipality [JCYJ20180306174037820]
- Science and Technology Planning Project of Guangdong Province [2016A020226032, 2017A020213008]
- Guangdong Basic and Applied Basic Research Foundation [2020A1515010058]
- Project of Administration of Traditional Chinese Medicine of Guangdong Province [20180326103756, 20190405225223]
- Shenzhen Key Medical Discipline Construction Fund [SZXK074]
- Innovation and Practice Base for Postdoctoral Researchers of Guangxi International Zhuang Medicine Hospital
Skeletal muscle atrophy in the aged causes loss in muscle mass and functions. Naturally occurring antioxidant flavonoid apigenin is able to ameliorate obesity- and denervation-induced muscle atrophies, but its effects on age-related muscle atrophy remain unknown. We hypothesized that apigenin can relieve muscle atrophy in aged mice, probably through special effects on reactive oxygen species and enzymes with antioxidant functions. For the male mice of the study, apigenin showed significant dose-dependent effects in relieving aging-related muscle atrophy according to results of frailty index as indicator of frailty associated with aging, grip strength, and running distance. Apigenin also improved myofiber size and morphological features and increased mitochondria number and volume, as manifested by succinate dehydrogenase staining and transmission electron microscopy. Our tests also suggested that apigenin promoted activities of enzymes such as superoxide dismutase and glutathione peroxidase for antioxidation and those for aerobic respiration such as mitochondrial respiratory enzyme complexes I, II, and IV, increased ATP, and enhanced expression of genes such as peroxisome proliferator-activated receptor-gamma coactivator 1 alpha, mitochondrial transcription factor A, nuclear respiratory factor-1, and ATP5B involved in mitochondrial biogenesis. The data also suggested that apigenin inhibited Bcl-2/adenovirus E1B 19kD-interacting protein 3 and DNA fragmentation as indicators of mitophagy and apoptosis in aged mice with skeletal muscle atrophy. Together, the results suggest that apigenin relieves age-related skeletal muscle atrophy through reducing oxidative stress and inhibiting hyperactive autophagy and apoptosis.
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