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Carvacrol protects the ARPE19 retinal pigment epithelial cells against high glucose-induced oxidative stress, apoptosis, and inflammation by suppressing the TRPM2 channel signaling pathways

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dc.creator Daldal, Hatice
dc.creator Nazirogluz, Mustafa
dc.date 2022-08-01T00:00:00Z
dc.date.accessioned 2023-01-09T12:07:52Z
dc.date.available 2023-01-09T12:07:52Z
dc.identifier c6b6c3f6-6fe1-4e6d-8c17-4f70aff2fed2
dc.identifier 10.1007/s00417-022-05731-5
dc.identifier https://avesis.sdu.edu.tr/publication/details/c6b6c3f6-6fe1-4e6d-8c17-4f70aff2fed2/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/98347
dc.description Purpose The concentration of plasma high glucose (HGu) in diabetes mellitus (DM) induces the retinal pigment epithelial cell (ARPE19) death via the increase of inflammation, cytosolic (cytROS), and mitochondrial (mitROS) free oxygen radical generations. Transient potential melastatin 2 (TRPM2) cation channel is stimulated by cytROS and mitROS. Hence, the cytROS and mitROS -mediated excessive Ca2+ influxes via the stimulation of TRPM2 channel cause to the induction of DM-mediated retina oxidative cytotoxicity. Because of the antioxidant role of carvacrol (CRV), it may modulate oxidative cytotoxicity via the attenuation of TRPM2 in the ARPE19. We aimed to investigate the modulator action of CRV treatment on the HGu-mediated TRPM2 stimulation, oxidative stress, and apoptosis in the ARPE19 cell model.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title Carvacrol protects the ARPE19 retinal pigment epithelial cells against high glucose-induced oxidative stress, apoptosis, and inflammation by suppressing the TRPM2 channel signaling pathways
dc.type info:eu-repo/semantics/article


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