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dc.contributor.authorAouichat, Samira
dc.contributor.authorNavarro Alarcón, Miguel 
dc.contributor.authorAlarcón Guijo, Pablo
dc.contributor.authorSalagre Simón, Diego 
dc.contributor.authorAgil Abdalla, Mhmad Ahmad 
dc.date.accessioned2021-04-23T08:19:53Z
dc.date.available2021-04-23T08:19:53Z
dc.date.issued2021
dc.identifier.citationAouichat, S.; Navarro-Alarcon, M.; Alarcón-Guijo, P.; Salagre, D.; Ncir, M.; Zourgui, L.; Agil, A. Melatonin Improves Endoplasmic Reticulum Stress-Mediated IRE1α Pathway in Zücker Diabetic Fatty Rat. Pharmaceuticals 2021, 14, 232. https://doi.org/10.3390/ph14030232es_ES
dc.identifier.urihttp://hdl.handle.net/10481/68066
dc.description.abstractObesity and diabetes are linked to an increased prevalence of kidney disease. Endoplasmic reticulum stress has recently gained growing importance in the pathogenesis of obesity and diabetesrelated kidney disease. Melatonin, is an important anti-obesogenic natural bioactive compound. Previously, our research group showed that the renoprotective effect of melatonin administration was associated with restoring mitochondrial fission/fusion balance and function in a rat model of diabesity-induced kidney injury. This study was carried out to further investigate whether melatonin could suppress renal endoplasmic reticulum (ER) stress response and the downstream unfolded protein response activation under obese and diabetic conditions. Zücker diabetic fatty (ZDF) rats and lean littermates (ZL) were orally supplemented either with melatonin (10 mg/kg body weight (BW)/day) (M–ZDF and M–ZL) or vehicle (C–ZDF and C–ZL) for 17 weeks. Western blot analysis of ER stress-related markers and renal morphology were assessed. Compared to C–ZL rats, higher ER stress response associated with impaired renal morphology was observed in C–ZDF rats. Melatonin supplementation alleviated renal ER stress response in ZDF rats, by decreasing glucose-regulated protein 78 (GRP78), phosphoinositol-requiring enzyme1α (IRE1α), and ATF6 levels but had no effect on phospho–protein kinase RNA–like endoplasmic reticulum kinase (PERK) level. In addition, melatonin supplementation also restrained the ER stress-mediated apoptotic pathway, as indicated by decreased pro-apoptotic proteins phospho–c–jun amino terminal kinase (JNK), Bax, and cleaved caspase-3, as well as by upregulation of B cell lymphoma (Bcl)-2 protein. These improvements were associated with renal structural recovery. Taken together, our findings revealed that melatonin play a renoprotective role, at least in part, by suppressing ER stress and related pro-apoptotic IRE1α/JNK signaling pathway.es_ES
dc.description.sponsorshipSpanish Government SAF2016-79794-Res_ES
dc.description.sponsorshipEuropean Commissiones_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rightsAtribución 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectMelatonines_ES
dc.subjectEndoplasmic reticulum stresses_ES
dc.subjectDiabesityes_ES
dc.subjectKidneys es_ES
dc.titleMelatonin Improves Endoplasmic Reticulum Stress-Mediated IRE1α Pathway in Zucker Diabetic Fatty Rates_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.identifier.doi10.3390/ph14030232


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