High-intensity interval training upregulates adiponectin receptor ۱ expression and modulates serum antioxidant enzymes in a Murine model of breast cancer

سال انتشار: 1405
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 61

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شناسه ملی سند علمی:

SPORTBCNF10_039

تاریخ نمایه سازی: 29 مرداد 1405

چکیده مقاله:

Aim: This study aimed to investigate the effects of high-intensity interval training (HIIT) on Adiponectin receptor ۱ (AdipR۱) gene expression in breast tumor tissue and serum levels of glutathione peroxidase (GPX) and glutathione reductase (GR) in a murine model of breast cancer. Methods: Sixteen male BALB/c mice were inoculated subcutaneously with ۴T۱ murine mammary carcinoma cells (۵ × ۱۰۵ cells/mouse). One week post-inoculation, mice were randomly assigned to either a tumor-bearing control group (Tumor, n=۸) or a tumor-bearing group subjected to HIIT (Tumor+HIIT, n=۸). The HIIT protocol was performed on a motor-driven treadmill five days/week for four weeks, consisting of six ۲-minute high-intensity intervals (۱۸-۲۵ m/min, ۸۰-۹۰% VO۲max) interspersed with ۳-minute active recovery periods (۵-۹ m/min). Twenty-four hours after the final session, tumor tissues were excised for AdipR۱ gene expression analysis via quantitative real-time PCR (۲^-AACT method), and serum samples were collected for assessment of GPX and GR levels using ELISA. Statistical comparisons were performed using independent samples t-tests (p<۰.۰۵). Results: HIIT significantly upregulated AdipR۱ gene expression in breast tumor tissue compared to the control group (p<۰.۰۰۰۱). Serum GPX levels were significantly decreased in the Tumor+HIIT group compared to the Tumor control group (p<۰.۰۰۰۱). However, no significant difference was observed in serum GR levels between the two groups (p=۰.۷۴۹۹). Conclusion: Four weeks of HIIT effectively enhanced AdipR۱ expression in tumor tissue and modulated the antioxidant profile by reducing serum GPX in tumor-bearing mice. These findings suggest that HIIT may influence breast cancer progression through adiponectin-mediated pathways and oxidative stress regulation, providing a potential non-pharmacological adjunctive strategy for breast cancer management. Further studies are warranted to elucidate the underlying molecular mechanisms and clinical implications.