Analysis of the Effects of Ninjin'yoeito on Physical Frailty in Mice.
Shotaro OtsukaKeita FukumaruAkira TaniSeiya TakadaKiyoshi KikuchiKosuke NorimatsuRyoma MatsuzakiTeruki MatsuokaHarutoshi SakakimaYuji OmiyaKeita MizunoYosuke MatsubaraIkuro MaruyamaPublished in: International journal of molecular sciences (2022)
Physical frailty is an aging-related clinical syndrome involving decreases in body weight, mobility, activity, and walking speed that occurs in individuals with sarcopenia and is accelerated by increased oxidative stress. Ninjin'yoeito, a traditional Japanese Kampo medicine, is used for treating conditions, including anemia and physical weakness. Here, we investigated whether ninjin'yoeito could improve physical frailty by controlling oxidative stress in the senescence-accelerated mouse prone 8 (SAMP8) model. First, SAMP8 mice were divided into two groups, ninjin'yoeito treated and untreated, with the former consuming a diet containing 3% ninjin'yoeito from 3 months of age. At 7 months of age, body weight, motor function, locomotor activity, and mean walking speed were measured. Subsequently, mice were euthanized and measured for muscle weight, 8-hydroxy-2'-deoxyguanosine levels in muscle and brain, and cleaved caspase-3 expression in brain. The results showed reductions in weight, locomotor function, locomotion, and average walking speed in the untreated group, which were significantly improved by ninjin'yoeito. Furthermore, 8-hydroxy-2'-deoxyguanosine levels were reduced in muscle and brain from ninjin'yoeito-treated mice, compared with the levels in untreated mice; cleaved caspase-3 expression was similarly reduced in brain from the treated mice, indicating reduced apoptosis. Our findings suggest that ninjin'yoeito inhibits sarcopenia-based physical frailty through its antioxidant effects.
Keyphrases
- body weight
- oxidative stress
- physical activity
- high fat diet induced
- skeletal muscle
- mental health
- poor prognosis
- cell death
- white matter
- resting state
- dna damage
- body mass index
- induced apoptosis
- weight loss
- endoplasmic reticulum stress
- type diabetes
- cerebral ischemia
- ischemia reperfusion injury
- metabolic syndrome
- functional connectivity
- heat shock
- weight gain
- signaling pathway
- subarachnoid hemorrhage
- stress induced
- heat shock protein