| 초록 |
Renal aging is characterized by cellular senescence, reduced function, and morphological alterations. Sodium-glucose cotransporter-2 (SGLT2) inhibitors have shown renoprotective effects beyond glycemic control in various kidney disease. This study evaluated the impact of SGLT2 inhibition on senescent changes in the aging kidney. Male C57/BL6 mice were used for aging mice model. 24-months-old mice were assigned to control group (n=7). Seven 19-month-old mice were treated with empagliflozin (10mg/kg/day) for 6 months, and were euthanized at age 24 months. We compared histological change, oxidative stress, and aging-related pro-inflammatory cytokines expression in the kidneys between empagliflozin treated group and control group. Empagliflozin-treated mice exhibited a significant reduction in senescence markers compared to controls, indicating an attenuation of renal cellular senescence. Although the treatment group had a lower overall body weight, their kidneys were significantly larger, suggesting preservation of renal mass. Moreover, serum creatinine levels were lower and eGFR values were higher in the empagliflozin group relative to controls. Histological evaluation revealed reduced tubular atrophy and interstitial fibrosis in treated mice. SGLT2 inhibition via empagliflozin over a 6-month period in aging mice ameliorates senescent changes in the kidney. This is evidenced by decreased expression of cellular senescence markers, increased kidney size despite lower body weight, and improved renal function parameters. These findings support the potential of SGLT2 inhibitors as a therapeutic strategy to delay renal aging and preserve kidney function in the elderly. |