GPX7 reduces chondrocyte inflammation and extracellular matrix degradation triggered by IL­1ß, via a mechanism mediated by ferroptosis.

During osteoarthritis (OA), chondrocytes become highly active, with increased matrix synthesis and inflammatory cytokine­induced catabolic pathways. Early intervention strategies targeting pathological changes may attenuate or halt disease progression. The present study aimed to reveal the role of glutathione peroxidase (GPX)7 in OA. For this purpose, a research model was established by inducing C28/I2 human chondrocytes with interleukin (IL)­1ß, and the expression level of GPX7 was determined. To explore its roles, C28/I2 cells were transfected to gain GPX7 overexpression. The effects of GPX7 overexpression on intracellular inflammation, extracellular matrix (ECM) degradation, apoptosis and ferroptosis were then evaluated. In addition, the cells were treated with the ferroptosis inducer, erastin, and its effects on the aforementioned phenotypes were assessed. The level of GPX7 was decreased in response to IL­1ß treatment, and GPX7 overexpression suppressed cellular inflammation, ECM degradation and apoptosis. Moreover, the reduction of lipid peroxidation, ferrous ions and transferrin indicated that GPX7 overexpression inhibited ferroptosis. Subsequently, inflammation, ECM degradation and apoptosis were found to be promoted in the cells upon treatment with erastin. These findings suggested that the regulatory role of GPX7 may be mediated by a pathway involving ferroptosis. On the whole, the present study revealed that GPX7 reduces IL­1ß­induced chondrocyte inflammation, apoptosis and ECM degradation partially through a mechanism involving ferroptosis. The results of the present study lay a theoretical foundation for subsequent OA­related research and may enable the development of translational strategies for the treatment of OA.

Effect of a moderate-intensity comprehensive exercise program on body composition, muscle strength, and physical performance in elderly females with sarcopenia.

Objective: This study aimed at examining an eight-week moderate-intensity comprehensive exercise training program on the parameters of sarcopenia in elderly females. Methods: A total of 49 community-dwelling elderly females with sarcopenia (65.5 ± 2.5) were assigned randomly to an experiment group (EG, n = 25) and a control group (CG, n = 24). In the EG, an eight-week comprehensive exercise training program was implemented, in 1 h, 3 times per week, a total of 24 sessions. The CG only received health public education per two weeks, a total of 4 times. Subsequently, the differences between the two groups were tested through two-way repeated ANOVA. Results: ASM, SMM, and SMI in the EG were significantly improved by 0.26 kg, 0.18 kg, and 0.10 kg/m2, respectively. Group-by-time interactions were significantly different on the ASM [F (1,47) = 6.25, η2 = 0.12] and SMI [F (1,47) = 6.77, η2 = 0.13]. Muscle strength was improved 0.8 kg in the EG. Significant group-by-time interaction differences were reported in the handgrip strength [F (1,47) = 6.8, η2 = 0.13] after the eight-week intervention. Compared with the baseline, gait speed was improved a 0.05 m/s and 5-time chair stand was decreased a 0.27 s in the EG. Group-by-time interactions were significantly different in 5-time chair stand [F (1, 47) = 6.35, η2 = 0.12]. Conclusions: The moderate-intensity comprehensive exercise was confirmed as a safe and convenient exercise program. Although a load of training intensity is not sufficient to improve the gait speed, this exercise protocol is promising in delaying overall results in community-dwelling sarcopenia elderly females and contributes to the improvement of muscle mass, handgrip strength, and 5TCS.