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1.
Biomedical and Environmental Sciences ; (12): 95-106, 2022.
Artículo en Inglés | WPRIM | ID: wpr-927639

RESUMEN

OBJECTIVE@#This study aimed to investigate the effects of caprylic acid (C8:0) on lipid metabolism and inflammation, and examine the mechanisms underlying these effects in mice and cells.@*METHODS@#Fifty-six 6-week-old male C57BL/6J mice were randomly allocated to four groups fed a high-fat diet (HFD) without or with 2% C8:0, palmitic acid (C16:0) or eicosapentaenoic acid (EPA). RAW246.7 cells were randomly divided into five groups: normal, lipopolysaccharide (LPS), LPS+C8:0, LPS+EPA and LPS+cAMP. The serum lipid profiles, inflammatory biomolecules, and ABCA1 and JAK2/STAT3 mRNA and protein expression were measured.@*RESULTS@#C8:0 decreased TC and LDL-C, and increased the HDL-C/LDL-C ratio after injection of LPS. Without LPS, it decreased TC in mice ( P < 0.05). Moreover, C8:0 decreased the inflammatory response after LPS treatment in both mice and cells ( P < 0.05). Mechanistic investigations in C57BL/6J mouse aortas after injection of LPS indicated that C8:0 resulted in higher ABCA1 and JAK2/STAT3 expression than that with HFD, C16:0 and EPA, and resulted in lower TNF-α, NF-κB mRNA expression than that with HFD ( P < 0.05). In RAW 264.7 cells, C8:0 resulted in lower expression of pNF-κBP65 than that in the LPS group, and higher protein expression of ABCA1, p-JAK2 and p-STAT3 than that in the LPS and LPS+cAMP groups ( P < 0.05).@*CONCLUSION@#Our studies demonstrated that C8:0 may play an important role in lipid metabolism and the inflammatory response, and the mechanism may be associated with ABCA1 and the p-JAK2/p-STAT3 signaling pathway.


Asunto(s)
Animales , Humanos , Masculino , Ratones , Transportador 1 de Casete de Unión a ATP/inmunología , Caprilatos/química , Colesterol/metabolismo , Dieta Alta en Grasa/efectos adversos , Inflamación/metabolismo , Janus Quinasa 2/inmunología , Metabolismo de los Lípidos/efectos de los fármacos , Macrófagos/inmunología , Ratones Endogámicos C57BL , Factor de Transcripción STAT3/inmunología , Transducción de Señal
2.
Indian J Cancer ; 2012 Jul-Sept; 49(3): 260-265
Artículo en Inglés | IMSEAR | ID: sea-144583

RESUMEN

Janus Activated Kinase (JAK) 2 plays an important role in the pathogenesis of myelofibrosis (MF). Ruxolitinib (INCB018424, Jakafi) is a potent dual JAK1 and JAK2 inhibitor. In November 2011, it became approved by the US FDA for the treatment of intermediate or high-risk MF. This review shall outline the role of Ruxolitinib in the current management of MF and its potential future.


Asunto(s)
Humanos , Janus Quinasa 1/inmunología , Janus Quinasa 1/metabolismo , Janus Quinasa 2/administración & dosificación , Janus Quinasa 2/inmunología , Janus Quinasa 2/metabolismo , Mielofibrosis Primaria/tratamiento farmacológico , Mielofibrosis Primaria/patología , Pirazoles/uso terapéutico
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