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1.
J Cell Biochem ; 119(1): 260-268, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28513976

RESUMO

During the early stages of atherosclerosis, monocytes bind and migrate into the endothelial layer, promoting inflammation within the aorta. In order to prevent the development of atherosclerosis, it is critical to inhibit such inflammation. The therapeutic effects of ginger have been investigated in several models of cardiovascular disease. However, although a number of previous studies have focused on specific compounds, the mechanisms of action responsible remain unclear. Here, we investigated five major compounds present in ginger, and observed that gingerenone A exhibited the strongest inhibitory effects against tumor necrosis factor (TNF)-α and lipopolysaccharide (LPS) induced monocyte-endothelial adhesion. Furthermore, gingerenone A significantly suppressed the expression of TNF-α and LPS-induced vascular cell adhesion molecule-1 (VCAM-1) and chemokine (C-C motif) ligand 2 (CCL2), key mediators of the interaction between monocytes, and endothelial cells. Transactivation of nuclear factor-κB (NF-κB), which is a key transcription factor of VCAM-1 and CCL2, was induced by TNF-α and LPS, and inhibited by treatment of gingerenone A. Gingerenone A also inhibited the phosphorylation of NF-κB inhibitor (IκB) α and IκB Kinase. Taken together, these results demonstrate that gingerenone A attenuates TNF-α and LPS-induced monocyte adhesion and the expression of adhesion factors in endothelial cells via the suppression of NF-κB signaling. J. Cell. Biochem. 119: 260-268, 2018. © 2017 Wiley Periodicals, Inc.


Assuntos
Diarileptanoides/farmacologia , Células Endoteliais da Veia Umbilical Humana/metabolismo , Quinase I-kappa B/metabolismo , Monócitos/metabolismo , Adesão Celular/efeitos dos fármacos , Células Cultivadas , Quimiocina CCL2/metabolismo , Células Endoteliais da Veia Umbilical Humana/citologia , Humanos , Lipopolissacarídeos/toxicidade , Monócitos/citologia , Fosforilação/efeitos dos fármacos , Fator de Necrose Tumoral alfa/metabolismo , Molécula 1 de Adesão de Célula Vascular/metabolismo
2.
Pak J Pharm Sci ; 28(1): 175-84, 2015 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-25553694

RESUMO

The aim of this work is to explore the protective of B vitamins (B(3), B(6) and B(12)) against the hepatotoxic potency of either bulk zinc oxide (ZnO-bulk) or its nanoparticles (ZnO-NPs)-induced liver damage in rats. ZnO- bulk or its NPs were administered orally (500 mg/kg b.w.) for 10 successive days. The results revealed that oral co-administration of combination of B vitamins (250 mg B(3), 60 mg B(6) and 0.6 mg B(12)/Kg body weight) daily for 3 weeks to rats intoxicated by either ZnO- bulk or its NPs markedly ameliorated increases in serum of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehdrogenase (LDH). The B vitamins also down-regulated increases in serum glucose level as well as increases in immuno-inflammatory biomarkers, including tumor necrosis factor-α (TNF-α) and C-reactive protein compared with intoxicated, untreated rats. Beside, the used agent successfully modulated the alterations in serum vascular endothelial growth factor (VEGF), attenuated liver oxidative DNA damage compared with ZnO intoxicated groups. We showed that the used B complex mitigated increased malondialdehyde (MDA), decrease in glutathione peroxidase (GPx) and increase in the apoptosis marker caspase 3 of liver tissue in response to either ZnO-bulk or its NP toxicity. In conclusion, early treatment with vitamin B complex may protect liver tissue from deleterious damage induced by the toxic effects of ZnO-bulk or its NPs.


Assuntos
Antioxidantes/farmacologia , Apoptose/efeitos dos fármacos , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Dano ao DNA , Fígado/efeitos dos fármacos , Nanopartículas Metálicas , Estresse Oxidativo/efeitos dos fármacos , Complexo Vitamínico B/farmacologia , Óxido de Zinco , Administração Oral , Animais , Antioxidantes/administração & dosagem , Biomarcadores/sangue , Doença Hepática Induzida por Substâncias e Drogas/sangue , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Doença Hepática Induzida por Substâncias e Drogas/patologia , Citoproteção , Mediadores da Inflamação/sangue , Fígado/metabolismo , Fígado/patologia , Masculino , Ratos Sprague-Dawley , Fatores de Tempo , Complexo Vitamínico B/administração & dosagem
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