Arman Ghorbani

Observational studies have reported inconsistent associations between hypothyroidism or hyperthyroidism and risk of liver cancer (LC). We therefore conduct

Oxidative stress plays a pivotal role in cellular aging, and dietary antioxidants may modulate this process through regulation of the aging-related Klotho gene. This cross-sectional study investigated the association between dietary total antioxidant capacity (DTAC) and Klotho gene expression in 50 healthy Iranian adults (aged 18–40 years). Using validated food frequency questionnaires, we calculated DTAC (mmol Trolox equivalents/day) and assessed Klotho mRNA levels in peripheral blood mononuclear cells (PBMCs) via RT-PCR (ΔCt method). Linear regression models evaluated these associations, with Model 1 showing crude associations and Model 2 adjusting for age, sex, BMI, waist circumference, physical activity, and fiber intake. Unadjusted analysis revealed DTAC significantly predicted Klotho expression (β = -0.662, p < 0.001, R² = 0.438), with higher antioxidant intake associated with lower ΔCt values (indicating greater Klotho expression). This association remained significant after full adjustment (β = -0.599, p = 0.002, Adjusted R² = 0.381). Notably, among individual antioxidants, only zinc maintained an independent inverse relationship with ΔCt Klotho in the adjusted model (β = -0.439, p = 0.016), while other antioxidants lost significance. These findings demonstrate that higher dietary antioxidant intake, particularly zinc, is significantly associated with increased Klotho gene expression, suggesting a potential mechanism by which antioxidant-rich diets may influence aging processes. This study provides novel evidence linking DTAC to Klotho expression in humans, supporting further investigation into dietary strategies for modulating aging-related pathways.

Background and Objectives: Fibroblast growth factor-21 (FGF-21) is a potent activator of glucose uptake associated with insulin resistance, metabolic syndrome and obesity. The aim of this study was to assess relationships between the anthropometric parameters, body composition, and FGF-21 gene expression in peripheral blood mononuclear cells in healthy young adults. Materials ...

Obesity, which is the accumulation of fat in adipose tissue, has adverse impacts on human health. Obesity-related metabolic dysregulation has similarities to the metabolic alterations observed in aging. It has been shown that the adipocytes of obese individuals undergo cellular aging, known as senescence. Senescence can be transmitted to other normal cells through a series of chemical factors referred to as the senescence-associated secretory phenotype (SASP). Most of these factors are pro-inflammatory compounds. The immune system removes these senescent T-cells, but immunosenescence, which is the senescence of immune cells, disrupts the clearance of senescent T-cells. Immunosenescence occurs as a result of aging or indirectly through transmission from senescent tissues. The significant occurrence of senescence in obesity is expected to cause immunosenescence and impairs the immune response to resolve inflammation. The sustained and chronic inflammation disrupts insulin's metabolic actions in metabolic tissues. Therefore, this review focuses on the role of senescent adipocyte cells in obesity-associated immunosenescence and subsequent metabolic dysregulation. Moreover, the article suggests novel therapeutic approaches to improve metabolic syndrome by targeting senescent T-cells or using senotherapeutics. Graphical Abstract

Egg peptides are factors in the embryonic environment with many significant biological activities, such as anticancer activity. Therefore, the current study investigates the effect of egg ovalbumin (OVA) on survival, cell cycle, self-renewal ability, stemness properties, and migration in SW480 colon cancer cells and 5-fluorouracil (5FU) resistant subgroup. MTT test was performed to assess cell viability. Flow cytometry was employed to analyze the cell cycle. Clonogenic assay and spheroid formation were used to assess the effect of OVA on self-renewal and stemness properties. Wound healing assay and RT-PCR were performed to analyze migration and gene mRNA expression. We demonstrated that OVA (8 and 12 mg/ml) attenuated cell viability, induced cell-cycle arrest, inhibited colony formation, and non-significantly reduced spheroid formation and migration in both cell lines. Furthermore, OVA downregulated the expression of Nanog, c-Myc, and NDRG1 in both cells, suggesting a stemness and self-renewal attenuation by OVA. In conclusion, OVA exposure inhibited the 5FU-SW480 chemo-resistant subpopulation growth by inducing cell cycle arrest and diminishing self-renewal and partially stemness properties of colon cancer cells.

The effect of thyroid hormone (TH) on cancers was proposed more than 100 years ago; however, conclusions are conflicting. THs are precisely regulated at tissue and cellular levels. It seems that this regulation is altered in cancers. Thyroid hormone receptor beta (TRβ) has anti-proliferative and tumor-suppressive effects in many cancer cells. Therefore, we decided to investigate thyroid hormone receptor beta (THRB) expression and activation by the selective agonist, GC-1, on tumor growth in a syngeneic mouse model of colorectal cancer (CRC) and colon cell lines. In vitro cell viability assay using MTT analysis, cell cycle analysis by PI staining, and FACS analysis were performed. In vivo tumor growth measurements were carried out by caliper and [¹⁸F] Fluoro-2-deoxy-2-D-glucose (FDG) – PET imaging. Gene expressions were determined using quantitative-PCR. Some concentrations of GC-1 had a marked negative effect on the cell viability of colorectal cell lines. Cell cycle analysis showed that the anti-proliferative effect of GC-1 may not result from cell cycle arrest or apoptosis. Tumor growth analysis in mice harboring colorectal tumor showed that GC-1 treatment for 8 d profoundly inhibited tumor growth and ¹⁸FDG uptake. THRB expression was decreased in mice tumor; however, it was upregulated following GC-1 administration. Our results showed that specific activation of TRβ by GC-1 had negative effect on tumor growth and restored its gene expression in tumors of CRC mice model.