PP133 - UMBELLIFERONE ATTENUATES SLIT DIAPHRAGM LOSS AND ACTIN CYTOSKELETAL INJURY IN HIGH GLUCOSE-EXPOSED PODOCYTES
PP133
UMBELLIFERONE ATTENUATES SLIT DIAPHRAGM LOSS AND ACTIN CYTOSKELETAL INJURY IN HIGH GLUCOSE-EXPOSED PODOCYTES
J. Kim1,*, M.-K. Kang2
1Department of Food and Nutrition, Changwon National University, Gyeongnam, 2Department of Food and Nutrition, Gyeongkuk National University, Gyeongsangbuk-do, Korea, Republic Of
Rationale: Podocyte injury is a key event in the development of albuminuria in diabetic nephropathy. Although umbelliferone (7-hydroxycoumarin), a plant-derived coumarin, has recognized anti-inflammatory and antioxidant activities, its direct effects on podocyte slit diaphragm integrity and cytoskeletal remodeling under hyperglycemic conditions remain unclear. This study investigated whether umbelliferone protects podocytes against high glucose-induced structural injury.
Methods: Podocytes were cultured for up to 4 days in 33 mM glucose, with 27.5 mM mannitol used as an osmotic control, in the presence or absence of umbelliferone (1-20 μM). Podocyte injury was assessed by examining slit diaphragm-related proteins, actin cytoskeletal markers, and Rho GTPase activity.
Results: High glucose induced podocyte injury characterized by loss of slit diaphragm integrity and disruption of actin cytoskeletal organization. Umbelliferone at non-cytotoxic concentrations dose-dependently attenuated these alterations. Umbelliferone restored the expression of slit diaphragm proteins, including podocin and nephrin, and increased the levels of F-actin and α-actinin-4 reduced by high glucose exposure. These protective effects were accompanied by modulation of Rho GTPase activity, suggesting involvement of cytoskeletal regulatory signaling.
Conclusion: Umbelliferone protected podocytes from hyperglycemia-induced structural damage by preserving slit diaphragm integrity and actin cytoskeletal organization. These findings provide mechanistic support for the renoprotective potential of a food-derived bioactive compound in diabetic nephropathy.
Disclosure of Interest: None declared