Accepted_test
This study investigates the geroprotective properties of urolithin A and its enhanced membranophilic derivative, KIRS152, in vitro. Aging is characterized by mitochondrial dysfunction and cellular senescence, processes intricately linked and central to aging phenotypes. Mitophagy, responsible for eliminating dysfunctional mitochondria, is explored as a potential therapeutic avenue for age-related diseases. Urolithin A, derived from ellagic acid, shows promise as a geroprotective and antioxidant agent, despite minimal uncoupling activity. The study aims to enhance urolithin A uncoupling properties to augment mitophagy induction and efficacy. Through the synthesis of KIRS152, a derivative with increased membranophilicity, the study seeks to compare the geroprotective effects of both compounds in a model of cisplatin-induced aging in human skin fibroblasts.
Methods involve assessing cytotoxicity and evaluating the impact of non-toxic concentrations of urolithin A and KIRS152 on senescence markers induced by cisplatin. Senescent phenotype markers include lipofuscin autofluorescence, cell diameter, senescence-associated β-galactosidase activity, and GDF15 secretion. Results indicate KIRS152's superior geroprotective effects compared to urolithin A, manifested through reduced senescence index and SA-β-gal-positive cells. Moreover, KIRS152 prevents increased GDF15 secretion induced by cisplatin, while displaying lower toxicity. The study highlights the potential of KIRS152 as a more effective geroprotective agent than urolithin A, implicating mitophagy/autophagy in their mechanisms and suggesting KIRS152's promise for combating age-related diseases.