The aim of this study is to elucidate the pharmacological mechanism underlying the effects of Ginseng Radix et Rhizoma (ginseng) in heart failure (HF), providing a theoretical foundation for its clinical application. The potential mechanism of ginseng in the context of HF was investigated using systems pharmacology that combined network pharmacology, Gene Expression Omnibus (GEO) analysis, molecular docking, and experimental verification. Network pharmacology was employed to identify drug-disease targets. Core gene targets were subsequently subjected to enrichment analysis by integrating network pharmacology with GEO. Molecular docking was utilized to predict the binding affinities between identified targets and ginseng compounds. Furthermore, the therapeutic efficacy of ginseng was validated in an isoproterenol (ISO)-induced rat model of HF. The modulation of key signaling pathways by ginseng was confirmed through Western blot analysis. A total of 154 potential targets of ginseng in the treatment of HF were identified through network pharmacology analysis. The analysis of GSE71613 revealed that the PI3K-Akt pathway, reactive oxygen species, oxidative phosphorylation, MAPK signaling, and Ras signaling pathways are predominantly associated with patients with HF. By integrating the findings from network pharmacology and GEO analysis, ginsenoside Rg1 and ginsenoside Rb3 were identified as the potential components in ginseng, while and were recognized as key targets involved in the PI3K-AKT and AMPK pathways, respectively. Molecular docking analysis revealed a strong affinity between the potential components and the identified core targets. experiments indicated that the extract of ginseng (EPG) significantly ameliorated ISO-induced cardiac dysfunction by improving cardiac parameters such as cardiac left ventricular internal systolic diameter, left ventricular end-diastolic volume, left ventricular end systolic volume, and left ventricular ejection fraction, while also reducing malondialdehyde production. In addition, EPG was found to enhance superoxide dismutase activity and ATP levels, while concurrently reducing the levels of interleukin (IL)-1β, IL-6, and TNF-α. The extract also reduced myocardial oxygen consumption, inflammatory cell infiltration, and the number of damaged myocardial fibers. Moreover, EPG was observed to upregulate the expression of p-PI3K, p-AKT, p-AMPK, and Bcl-2, while downregulating the expression of p-NFκB, TGF-β, and Bax. The therapeutic effects of ginseng on HF are primarily mediated through the PI3K-Akt and AMPK pathways. Ginsenoside Rg1 and ginsenoside Rb3 have been identified as potential therapeutic agents for HF.

In-stent restenosis (ISR) commonly occurs in elderly patients with coronary artery disease (CAD) after percutaneous coronary intervention. Atherosclerosis in elderly patients may be the leading cause of ISR. Therefore, we aim to explore the relationship between vascular calcification-associated factors and ISR occurrence. Elderly patients were enrolled according to standard inclusion and exclusion criteria. The serum fibroblast growth factor 23 (FGF23), hypoxia-inducible factor-1α (HIF-1α), and Klotho levels were determined using an enzyme-linked immunosorbent assay. The degree of coronary artery stenosis of the patients with CAD before operation was assessed using the Gensini score. The correlation was analyzed using Pearson analysis. The prediction value was evaluated using receiver operating characteristic (ROC) curve analysis. The patients with CAD were classified into the ISR group with 97 cases and the non-ISR (NISR) group with 349 cases. The Gensini score, serum FGF23, and HIF-1α levels increased while Klotho levels decreased in patients with CAD of the ISR group compared with those of the NISR group. Pearson analysis showed that FGF23 and HIF-1α positively correlated while Klotho negatively correlated to the Gensini score. ROC analysis showed all three factors could effectively predict the occurrence of ISR. Furthermore, the joint had a more effective prediction value for ISR occurrence. The dynamic analysis presented that the serum FGF23 and HIF-1α levels dramatically increased while Klotho levels decreased in patients with CAD after 1-year follow-up. Serum FGF23 and HIF-1α positively correlated while serum Klotho negatively correlated to ISR. Conclusively, these three factors effectively predicted the occurrence of ISR.

Elderly individuals represent a significant demographic undergoing total hip arthroplasty, with distinct risks and complications. The study aimed to determine whether predictive nursing, guided by risk assessment, could reduce these risks and improve patient outcomes. A total of 191 elderly patients undergoing total hip arthroplasty were included in the study, with 142 patients randomly assigned to either the control or observation groups. The control group received routine care, while the observation group received predictive nursing based on comprehensive risk assessment. Various assessment tools were employed to evaluate risks such as venous thrombosis, pressure injuries, falls, joint dislocation, infections, and psychological factors. The primary outcomes included functional improvement measured by the Harris Hip Score, Activities of Daily Living (ADL), anxiety levels, and patient satisfaction. Our study demonstrated that predictive nursing interventions, guided by comprehensive risk assessment, yielded significant reductions in postoperative complications, particularly deep vein thrombosis, in elderly patients undergoing total hip arthroplasty. In addition, patients who received predictive nursing care experienced notable benefits, including shorter hospital stays, heightened satisfaction levels, enhanced hip function, improved ADL scores, and reduced anxiety levels compared with those receiving standard care. The study underscores the substantial benefits of predictive nursing interventions guided by risk assessment in improving outcomes for elderly patients undergoing total hip arthroplasty, highlighting the potential of individualized nursing care to optimize postoperative recovery and enhance patient well-being.

Chronic inflammation (inflammaging) is one of the important reasons for the development of age-related diseases and aging. Carrying out aging research and mining inflammatory markers can develop antiaging intervention targets, thus promoting healthy aging. By comparing the levels of inflammatory proteome in the serum of Chinese long-living people over 90 years and elderly aged 60∼79 which was detected by Olink platform, this study found that some pro-inflammatory or pro-aging proteins increased significantly in the long-living people, such as c-x-c motif chemokine ligand 9, accompanied by a significant increase in the levels of several anti-inflammatory or antiaging proteins, including fibroblast growth factor 19 and fibroblast growth factor 23, which confirmed that compared with elderly people, pro-inflammatory and anti-inflammatory (pro-aging and antiaging) tend to be balanced in long-living people, thus reducing the risk of age-related diseases and prolonging the lifespan of the elderly. These differently expressed proteins could serve as therapeutic targets and monitoring indicators for antiaging. At the same time, a few inflammatory protein markers, especially c-x-c motif chemokine ligand 9 and osteoprotegerin, could distinguish long-living and elderly correctly, which could be used to predict lifespan combined with other antiaging markers.

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 -23b-3p targeted MST1 and inhibited its expression. Overexpression of -23b-3p inhibited MST1 levels, thereby reducing cellular ferroptosis and attenuating MPP-induced cell injury. Collectively, MST1 expression increased with increasing MPP concentration, and -23b-3p targeted MST1 to reduce ferroptosis and MPP-induced cell injury.

Lipofuscin is indigestible garbage that accumulates in the autophagic vesicles and cytosol of postmitotic cells with age. Drs. Brunk and Terman postulated that lipofuscin accumulation is the main or at least a major driving factor in aging. They even posited that the evolution of memory is the reason why we get lipofuscin at all, as stable synaptic connections must be maintained over time, meaning that the somas of neurons must also remain in the same locale. In other words, they cannot dilute out their garbage over time through cell division. Mechanistically, their position certainly makes sense given that rendering a large percentage of a postmitotic cell's lysosomes useless must almost certainly negatively affect that cell and the surrounding microenvironment. It may be the case that lipofuscin accumulation is the main issue with regard to current age-related disease. Degradation may be an insurmountable task currently. However, a method of systemic lipofuscin removal is discussed herein.

Liver fibrosis is a commonly observed pathological phenomenon that occurs during the progression of various types of chronic liver diseases. The Hippo pathway is closely associated with the pathogenesis of liver fibrosis. Previous studies have shown that wedelolactone (WED) has a significant antihepatic fibrosis effect, whereas the target and mechanism underlying WED remain elusive. In this study, we found that WED significantly alleviated liver fibrosis and injury by inhibiting the expression of Yes-associated protein (YAP) and tafazzin (TAZ). In an model, WED suppressed the activation of hepatic stellate cells (HSCs) induced by transforming growth factor (TGF-β1), as well as the mRNA and protein expression of α-smooth muscle actin (α-SMA), YAP, and TAZ. The allosteric regulation of YAP by WED was confirmed using MD and cellular thermal shift assay. Moreover, specific knockdown or inhibition of YAP did not enhance the suppressive effect of WED on HSC activation or protein expression associated with fibrosis. These findings demonstrated that the administration of WED effectively alleviated liver fibrosis by suppressing the Hippo/YAP/TAZ pathways. In addition, YAP activity may be regulated by WED via allosteric regulation.

Arterial stiffness is an emerging indicator of cardiovascular risk, but its causal relationship with a variety of age-related diseases is unclear. The objective is to assess the causal relationship between arterial stiffness index (ASI) and age-related diseases by Mendelian randomization (MR) analysis. We obtained instrumental variables associated with age-related diseases from genome-wide association studies (GWAS) of 484,598 European individuals, and data for ASI were obtained from the UK Biobank GWAS of 127,127 participants. We used the inverse variance-weighted as the primary analysis method. In addition, several sensitivity analyses including MR-Egger, weighted-median (WM), Mendelian randomization pleiotropy residual sum and outlier, and Cochran's Q test were performed to test the robustness of the results. Reverse MR analysis was also performed to assess reverse causal relationships between age-related diseases and ASI. We verified the causal relationship between eight age-related diseases and ASI, of which cardiovascular disease ( = 0.19), gallbladder disease ( = 0.85), liver, biliary, or pancreas problem ( = 1.02), hypertension ( = 0.19), joint disorder ( = 0.53), and esophageal disorder ( = 2.10) elevated ASI. In contrast, hyperthyroidism or thyrotoxicosis ( = -2.17) and bowel problems ( = -1.83) may reduce ASI. This MR analysis reveals causal relationships between ASI and several age-related diseases. ASI is expected to be a potential indicator of health conditions for older populations.

Parishin, a natural compound, has demonstrated significant potential in mitigating age-related phenotypes and improving outcomes in age-associated diseases. Given that aging is a major risk factor for numerous chronic conditions, including pulmonary fibrosis, we investigated parishin's effects on cellular senescence and lung health. In our study, we treated mouse lung epithelial cells with parishin and observed a reduction in cellular senescence markers alongside an upregulation of sirtuin 1 (SIRT1). Building on these findings, we administered parishin to naturally aged mice. The treatment resulted in decreased pulmonary fibrosis and reduced DNA damage in lung tissue. Notably, we found that parishin treatment led to a reduction in Cluster of differentiation 38 (CD38) levels, concomitant with an increase in SIRT1 expression. These findings indicate that parishin may enhance lung function in aged mice, suggesting its potential as a therapeutic agent for treating age-related pulmonary disorders.

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 CD4T and CD8T 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 CD4T and CD8T 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, CD4T expression in the moxibustion group was downregulated, while CD8T 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, CD4T expression in the moxibustion group was decreased, while CD8T expression was increased. The results demonstrate that moxibustion not only suppressed the expression of CD4T but also promoted the expression of CD8T. The anti-inflammatory effect of moxibustion may be related to the regulation of T cell expression through the Tim-3/Gal-9 signaling pathway.

NQO1 disruption enhances susceptibility to oxidative stress during hyperglycemia and is a significant contributor to the development and progression of diabetes. Oxidative stress has been linked to several symptoms, including hyperglycemia, reactive oxygen species buildup, high blood pressure, and the expression of inflammatory markers. Therefore, the present research aimed to evaluate the genetic abnormality of NQO1 (rs1800566, C609T) gene polymorphism, expression, and vitamin-D level assessment among Type 2 diabetes mellitus (T2DM) patients. The study included 100 newly diagnosed T2DM cases and 100 healthy individuals as healthy controls. Total RNA was extracted from the whole blood using the TRIzol method, and further cDNA was synthesized, and expression was evaluated. There is a significant difference in NQO1 (rs1800566, C609T) genotype distribution among the T2DM patients and healthy controls ( = 0.04). Compared with the NQO1 CC wild-type genotype, the NQO1 CT heterozygous genotype had an odds ratio of 1.96 (1.08-3.55), and the NQO1 TT mutant type genotype had an odds ratio of 3.31 (0.61-17.77). Significantly decreased expression of NQO1 mRNA was observed with heterozygous CT ( < 0.0001) and homozygous mutant TT genotype ( = 0.0004), compared with homozygous wild-type CC genotype. NQO1 mRNA expression level was also compared with vitamin D levels among the T2DM patients. T2DM patients with vitamin D deficiency had 1.83-fold NQO1 mRNA expression, while vitamin D insufficient and sufficient T2DM cases had 3.31-fold ( < 0.0001) and 3.70-fold ( < 0.0001) NQO1 mRNA expression. It was concluded that NQO1 (rs1800566, C609T) CT and TT genotypes played a significant role in the worseness of type II diabetes mellitus, and decreased expression of NQO1 mRNA expression could be an essential factor for disease worseness as well as hypermethylation could be a factor for reduced expression leading to disease severity. The decreased NQO1 mRNA expression with heterozygous CT and mutant TT genotype associated with vitamin D deficiency may contribute to disease progression.

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 ( < 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 ( < 0.001), increased body fat percentage ( < 0.05), increased waist circumference ( < 0.05), reduced fat-free mass ( < 0.05), decreased lower limb flexibility ( < 0.05), and declined cardiorespiratory fitness ( < 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 ( < 0.05) were significantly associated with the reversal of frailty subtypes ( < 0.05). Younger older adults ( < 0.001), males ( < 0.05), those with lower WHO Disability Scale scores ( < 0.05), and higher MMSE scores ( < 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.

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), = 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.

Pathogenesis of vascular dementia (VD) is still unclear, there are currently no effective prevention and treatment methods. We applied Mendelian randomization (MR) using summary statistics from large-scale GWAS of metabolites and VD to reveal the causal effect of metabolites on the VD. One set of genetics instrument was used for analysis, derived from publicly available genetic summary data. Which was 32 single-nucleotide polymorphisms robustly associated with metabolites. Inverse-variance weighted, weighted median method, MR-Egger regression, and MR Pleiotropy RESidual Sum and Outlier test were used for MR analyses. Strong evidence for a positive effect of metabolites, which means N6-threonylcarbamoyladenosine (tA) on VD was found in inverse-variance weighted (odds ratios [OR]: 0.667, 95% confidence interval [CI]: 0.548-0.812, < 0.001), MR-Egger (OR: 0.647, 95% CI: 0.458-0.913, = 0.019), and weighted median (OR: 0.650, 95% CI: 0.466-0.908, = 0.012). The MR analysis indicated that metabolites (tA) may be causally associated with a positive effect on VD.

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.

This study aims to investigate the expression differences of peripheral blood mononuclear cells (PBMCs) in patients with elderly rheumatoid arthritis (ERA). Differentially expressed genes (DEGs) of PBMCs between young patients with RA (RA_Y) and elderly patients with RA (RA_A) were identified by RNA sequencing using the package, followed by bioinformatics analysis. The overlapped targets of the current DEGs and proteomic differentially expressed proteins (another set of unpublished data) were identified and further validated. The bioinformatics analysis revealed significant transcriptomic heterogeneity between RA_A and RA_Y. A total of 348 upregulated and 363 downregulated DEGs were identified. Gene functional enrichment analysis indicated that the DEGs, which represented senescence phenotype for patients with ERA, were enriched in pathways such as Phosphatidylinositol3 kinase/AKT serine-threonine protein kinase (PI3K/Akt) signaling, Mitogen-activated protein kinases (MAPK) signaling, toll-like receptor family, neutrophil degranulation, and immune-related pathways. Gene set enrichment analysis further confirmed the activation of humoral immune response pathways in RA_A. Quantitative polymerase chain reaction validated the expression of five representative DEGs such as , , , , and in PBMCs of patients with ERA. Patients with ERA have significant senescence phenotype differences versus the young patients. The DEGs identified may facilitate exploring the biomarkers of senescence in RA.

Geroscience, or longevity biotechnology, has made impressive advances in recent years that have led to the founding of dozens of start-ups, nonprofits and advocacy organizations, and the formation of a global movement to defeat aging. The community envisions changes at the regulatory and policy levels and calls for increased funding for research. Nevertheless, progress in the field has not been matched by discussions about ethical, legal, and social implications, as longevity advocates assume that seeking to expand lifespan or health span is inherently desirable and permissible. In this article, I make the case for the importance of putting ethics and society back into geroscience, along with three considerations for the longevity community. First, it should seek to understand the needs and attitudes of the public. Second, the community needs to define whether the field is primarily striving for healthy aging (increasing ) or for extending years of life (). Third, it needs to define the role of investors and tech millionaires in shaping the field's priorities and direction. This last point raises the question of who is setting the direction of a field that can reshape the meaning of being human.

This study aimed to explore the effects of the cluster nursing strategy applied to traumatic brain injury (TBI) patients. Ninety-eight TBI patients admitted to the hospital were selected as the study subjects. They were randomized into two groups, the control group and the cluster group, with 49 cases in each group. The control group received routine nursing methods, while the cluster group received cluster nursing strategy. The intervention effects were compared between the two groups. After 3 months, the total occurrence of complications in the cluster group was significantly lower than that in the control group. Postintervention, the cluster group had a significantly lower National Institutes of Health Stroke Scale score and significantly higher Fugl-Meyer score and Loewenstein Occupational Therapy Cognitive Assessment score compared with the control group. The serum level of glial fibrillary acidic protein in the control group was significantly higher than that in the cluster group, while the serum level of brain-derived neurotrophic factor was significantly lower. The application of the cluster nursing strategy in the care of patients with TBI could effectively reduce the risk of complications and improve neurological, motor, and cognitive functions.

Oxidative stress (OS) causes biochemical and morphological alterations in erythrocytes. The primary factors contributing to OS are aging and storage. Antioxidants significantly alleviate OS. Therefore, this study aimed to investigate the response of young and old erythrocytes to vitamin C and vitamin E during storage. Erythrocytes were separated into young and old by the Percoll method. Each erythrocyte subpopulation was categorized into the i) Control (additive solution-7 [AS-7]) and ii) vitamin C and vitamin E in AS-7 (VC+VE) groups and stored for 21 days at 4°C. OS, antioxidant, and aging markers were analyzed on days 1, 14, and 21. The activity of antioxidant enzymes was similar throughout storage in young cells. However, superoxide dismutase activity elevated in old cells (Control and VC+VE) on days 1 and 21. Catalase (CAT) activity increased on days 14 and 21, whereas glutathione peroxidase (GPX) increased on days 1 and 14 in old Controls. However, in old VC+VE, CAT increased on day 21 and GPX increased on day 1. Advanced oxidation protein products, superoxides, glutathione, and uric acid increased in old cells throughout storage. Malondialdehyde decreased in old VC+VE compared with old Control on days 14 and 21. Sialic acids and glutamate oxaloacetate transaminase activity were higher in young cells compared to old cells. Young cells exhibited lower oxidative changes throughout storage. Vitamin C and vitamin E were effective in maintaining the redox balance in old cells. These findings emphasize the need for specific approaches for different subpopulations during erythrocyte banking.