Hepatoprotective Effects of Swimming Exercise against D-Galactose-Induced Senescence Rat Model

This study investigates whether a 12-week swimming exercise training can prevent liver damage or senescence associated biomarkers in an experimental aging model in rats. Twenty-three male Sprague-Dawley rats were divided into four groups: vehicle treatment with sedentary control (C, n = 6), aging induction with sedentary (A, n = 6), vehicle treatment with swimming exercise (SW, n = 5), and aging induction with swimming exercise (A + SW, n = 6). Rats in groups A and AS received intraperitoneal d -galactose injections (150 mg/kg/day) for 12 weeks to induce aging. Rats in groups SW and A + SW were subjected to swimming exercise training for 12 weeks. Body weight, liver weight, epididymal fat mass, blood biochemistry, and liver pathology were performed at the end of the experiment. Hepatic senescence protein markers such as β -galactosidase, p53, and p21, as well as the inflammatory mediator, IL-6, were examined. The d -galactose-treated rats exhibited increases in AST and γ -GT plasma levels and β -galactosidase protein expression compared to the control group. Swimming exercise significantly reduced BW, epididymal fat mass, γ -GT activity, and p53, p21, and IL-6 protein levels compared to the aging group. These results suggest that a 12-week swimming exercise program suppresses senescence markers and downregulates inflammatory mediator in the liver tissues of d -galactose-induced aging rats.