Rejuvenation research最新文献

To observe the effects of moxibustion on T cells and T cell immunoglobulin and mucin-domain-containing molecule-3/galectin-9 (Tim-3/Gal-9) pathway in rats with rheumatoid arthritis (RA). To further explore the possible anti-inflammatory mechanism of moxibustion in the treatment of RA. Thirty Sprague Dawley rats were randomly divided into three groups, including a control group, an RA model group, and a moxibustion group. An RA model was created through the injection of Freund's complete adjuvant. In the moxibustion group, rats were treated with moxibustion at acupoints of "Shenshu" and "Zusanli." A total of three courses of treatment were conducted. Then the thickness of foot pad was measured, joint pathological changes were observed by hematoxylin-eosin (HE) staining, the proportion of CD4⁺T and CD8⁺T in peripheral blood was detected by flow cytometry, the expression levels of Tim-3 and Gal-9 in synovium were detected by polymerase chain reaction (PCR), and the expressions of CD4⁺T and CD8⁺T in synovium were detected by immunofluorescence. HE staining showed that the synovial tissue of the control group was smooth and neatly arranged without inflammatory cell infiltration. In the model group, the joint space was narrowed, the synovial tissue had congestion and edema, and a large number of inflammatory cells infiltrated. Compared with the model group, in the moxibustion group, the joint space narrowed with synovium hyperemia and edema, and the level of inflammatory cell infiltration decreased. Flow cytometry showed that compared with the model group, CD4⁺T expression in the moxibustion group was downregulated, while CD8⁺T expression was upregulated. PCR results showed that compared with the model group, the expressions of Tim-3 and Gal-9 in the moxibustion group were upregulated. Immunofluorescence results showed that compared with the model group, CD4⁺T expression in the moxibustion group was decreased, while CD8⁺T expression was increased. The results demonstrate that moxibustion not only suppressed the expression of CD4⁺T but also promoted the expression of CD8⁺T. The anti-inflammatory effect of moxibustion may be related to the regulation of T cell expression through the Tim-3/Gal-9 signaling pathway.

Aging-related muscle atrophy/sarcopenia is the most common type of muscle impairment that affects the quality of life. In the current study, we examined the effect of a functional food mixture of amla, turmeric, black pepper, cinnamon, and ginger on D-galactose-induced muscle alterations in rats. Wistar rats were randomly divided into three groups: Control (C), D-galactose (G), and D-galactose + functional food mixture intervention (G + I). Rats in group-G and -G + I were injected with D-galactose (300 mg/kg/day) for 90 days. After 3 months of the experimental period, the rats were sacrificed to collect gastrocnemius muscle. Group-G rats showed elevated levels of inflammatory cytokines (TNFα and NF-kB), atrogenes (atrogin-1 and MuRF1), decreased insulin/IGF1 signaling (decreased AKT phosphorylation), altered mitochondrial dynamics (increased fission and decreased fusion proteins), increased apoptotic mediators (Bax/Bcl-2, and caspase-3), and decreased muscle cell cross-sectional area when compared with group-C (p < 0.05). Interestingly, supplementation with the functional food mixture prevented galactose-induced alterations in the muscle. The observed anti-inflammatory, insulin-sensitizing, mitochondria-protective, and antiapoptotic effects of the functional food could be the underlying mechanisms in displaying positive effects against galactose-induced muscle atrophy and, hence, may be useful for the prevention of age-related muscle disorders.

Frailty, a multifaceted syndrome, affects approximately 26% of older adults globally, yet there are limited data on the prevalence and longitudinal impact of frailty subtypes. Therefore, in this study, we aim to determine the prevalence of physical, psychological, and cognitive frailty, transitions between subtypes, and associated health determinants among Malaysian community-dwelling older adults. This study is part of the longitudinal aging study in Malaysia (LRGS Ageless and TUA). We assessed 815 older adults in 2014, with successful follow-up of 402 participants (mean age: 67.08 ± 5.38 years) after 5 years. Frailty subtypes were assessed at baseline, and transitions were evaluated at the 5-year mark. At baseline, the prevalence of older adults categorized as robust, physical frailty, cognitive frailty, and psychological frailty was 26.7%, 36.3%, 12.1%, and 16.7%, respectively, with 8.1% exhibiting concurrent psychological and cognitive frailty. Follow-up results showed that 22.9% remained robust, 46.8% experienced no change, 24.9% deteriorated (adversed), and 5.5% improved (reversed). Logistic regression analysis identified living alone (p < 0.001), increased body fat percentage (p < 0.05), increased waist circumference (p < 0.05), reduced fat-free mass (p < 0.05), decreased lower limb flexibility (p < 0.05), and declined cardiorespiratory fitness (p < 0.05) as significant predictors of frailty deterioration. Higher Mini Mental State Examination (MMSE) scores and improved Timed Up and Go and Chair Stand test results (p < 0.05) were significantly associated with the reversal of frailty subtypes (p < 0.05). Younger older adults (p < 0.001), males (p < 0.05), those with lower WHO Disability Scale scores (p < 0.05), and higher MMSE scores (p < 0.05) were significantly less likely to develop frailty subtypes. Intervention strategies that focus on combined physical, cognitive, and psychosocial functions are crucial for both reversing and preventing the progression of frailty subtypes in older adults.

Aging is an inevitable biological process that significantly impacts human health, leading to a decline in cellular function and an increase in cellular damage. This study elucidates the burgeoning potential of antiaging pharmaceuticals in mitigating the thriving burden of chronic conditions linked to advancing age. It underscores the pivotal role of these pharmacotherapeutic agents in fostering longevity free from debilitating age-related afflictions, notably cardiovascular disorders, neoplastic processes, and neurodegenerative pathologies. While commendable strides have been made evident in preclinical models, it is crucial to thoroughly investigate their effectiveness and safety in human groups. In addition, ethical concerns about fair access, societal impacts, and careful resource distribution are significant in discussions about developing and using antiaging medications. By approaching the development and utilization of antiaging medications with diligence and foresight, we can strive toward a future where individuals can enjoy extended lifespans free from the debilitating effects of age-related ailments.

Exploring the causal relationship between sarcopenia and neoplasm of bone and articular cartilage (NBAC) by bidirectional Mendelian randomization (MR). Genome-wide association study (GWAS) data on sarcopenia-associated traits including appendicular lean mass, low handgrip strength (including criteria from the European Working Group on Sarcopenia in Older People and the Foundation for the National Institutes of Health), and usual walking speeds were obtained from the UK Biobank. GWAS data for NBAC (benign and malignant) were provided by the Finnish Genetic Database. Three different methods of MR analysis, including inverse-variance weighted, Mendelian randomized Egger regression, and weighted median methods, were utilized. MR analysis showed that high appendicular lean mass was positively associated with the risk of developing benign NBAC (odds ratio and 95% confidence interval = 1.236 (1.026,1.489), p = 0.025). At the same time, there is no statistically significant association was found between traits related to sarcopenia and malignant neoplasm of bone and articular cartilage. There was also no reverse causal correlation between NBAC and traits related to sarcopenia. In European populations, better appendicular lean body mass is positively associated with the risk of benign neoplasm of bone and articular cartilage, representing the possibility that sarcopenia may be a protective factor against neoplasm of bone and articular cartilage.

Parkinson's disease (PD) is a multifactorial degenerative disease in the elder. Given the involvement of mammalian sterile 20-like kinase 1 (MST1) in PD, this article was to illustrate the mechanism of MST1 in 1-methyl-4-phenylpyridinium ion (MPP⁺)-induced PD cell model. Cells were treated with different concentrations of MPP⁺ to establish a PD cell model. Reverse transcription-quantitative polymerase chain reaction and Western blot revealed that MST1 expression and iron ion concentration increased, but cellular viability decreased with MPP⁺ concentration. Inhibition of MST1 decreased ferroptosis; increased cellular viability, iron ion content, and levels of glutathione peroxidase 4; and decreased reactive oxygen species and lactate dehydrogenase release. Upregulation of ferroptosis levels using ferroptosis agonist Erastin reduced the protective effect of MST1 inhibition on PD cells. Mechanistically, dual-luciferase analysis identified that miR-23b-3p targeted MST1 and inhibited its expression. Overexpression of miR-23b-3p inhibited MST1 levels, thereby reducing cellular ferroptosis and attenuating MPP⁺-induced cell injury. Collectively, MST1 expression increased with increasing MPP⁺ concentration, and miR-23b-3p targeted MST1 to reduce ferroptosis and MPP⁺-induced cell injury.