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作 者:LUCIANA MAZZEI MARÍA BELÉN RUIZ-ROSO NATALIA DE LAS HERAS SANDRA BALLESTEROS CAROLINA TORRESPALAZZOLO LEÓN FERDER ALEJANDRA BEATRIZ CAMARGO WALTER MANUCHA
机构地区:[1]Instituto de Medicina y Biología Experimental de Cuyo(IMBECU),Consejo Nacional de Investigaciones Científicas y Tecnológicas(CONICET),Mendoza,5500,Argentina [2]Área de Farmacología,Departamento de Patología,Facultad de Ciencias Médicas,Universidad Nacional de Cuyo Centro Universitario,Mendoza,5500,Argentina [3]Departamento de Fisiología,Facultad de Medicina,Universidad Complutense,Madrid,34523,España [4]IBAM,Universidad Nacional de Cuyo,CONICET,Facultad de Ciencias Agrarias,Mendoza,M5528AHB,Argentina [5]Department of Pediatrics,Nephrology Division,Miller School of Medicine,University of Miami,Miami,33012,USA
出 处:《BIOCELL》2020年第4期671-681,共11页生物细胞(英文)
基 金:Secretaría de Ciencia,Técnica y Postgrado,Universidad Nacional de Cuyo,and from ANPCyT(Agencia Nacional de Promoción de la Ciencia y la Tecnología,grant number PICT 2016-4541);both awarded to W.Manucha.
摘 要:The ancestral cultures have described many therapeutic properties of garlic,therefore,it is of central interest to elucidate the molecular basis explaining this millenary empirical knowledge.Indeed,it has been demonstrated a neuroprotective effect of allicin–a phytochemical present in garlic-linked to oxidative-inflammatory modulation.Allicin improved neuronal injury by heat shock protein 70(Hsp70)and inducible nitric oxide synthase(iNOS)regulation.Also,allicin exerts renal protection involving a possible angiotensin type 1 receptor(AT1)interaction.In connection,AT1 overexpression has been recognized as a central deleterious factor in many brain diseases.However,there are no studies that evaluate AT1-Hsp70-iNOS interaction as a mechanism linked to neuroinflammation.Thus,our central aim is to evaluate if the allicin protective effect is associated with an AT1-Hsp70-iNOS counterbalance axis.For this study,a murine microglial cell line(BV-2)was injured with lipopolysaccharides and treated or not with allicin.Then,it was evaluated cell viability,proinflammatory cytokine levels,cellular oxidative stress,iNOS,Hsp70,and AT1 protein expression(cellular and mitochondrial fractions),nitrite levels,and protein-protein interactions.The results demonstrated that allicin could prevent neuronal injury due to a reduction in oxidative stress and inflammatory status mediated by an AT1-Hsp70-iNOS counterbalance axis linked to direct protein-protein interaction.
关 键 词:ALLICIN NEUROINFLAMMATION BV-2 cells AT1 receptors INOS HSP70
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