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1.
Acta cir. bras ; Acta cir. bras;33(6): 542-550, June 2018. tab, graf
Artículo en Inglés | LILACS | ID: biblio-949355

RESUMEN

Abstract Purpose: To evaluate the effects of 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) on the content of triglyceride (TG), as well as on the gene and protein expressions of adiponectin receptor 2 (AdipoR2), p38 mitogen-activated protein kinase (P38MAPK), and lipoprotein lipase (LPL) in the liver of rats with type 2 diabetes mellitus (T2DM) so as to provide theoretical basis for exploring the mechanism by which 1,25(OH)2D3 regulates TG. Methods: Wistar rats were divided into four groups (n=25), with different treatments and detected the gene and protein expressions of AdipoR2, p38MAPK, and LPL in the liver tissue by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Meanwhile, the content of TG in the liver tissue was detected by the Enzyme-linked immunosorbent assay. Results: The expression of AdipoR2, p38MAPK, LPL gene and protein in the liver of VitD intervention group was significantly higher than that in T2DM group (P <0.05), while the TG content was significantly lower than that in T2DM group (P <0.05). Conclusion: 1,25(OH)2D3 can decrease the content of TG in the liver, and its mechanism may be achieved by upregulating the expressions of AdipoR2, p38MAPK, and LPL in the liver.


Asunto(s)
Animales , Masculino , Triglicéridos/sangre , Calcitriol/farmacología , Diabetes Mellitus Tipo 2/metabolismo , Hígado/efectos de los fármacos , Hígado/metabolismo , Valores de Referencia , Glucemia/análisis , Peso Corporal , Ensayo de Inmunoadsorción Enzimática , Expresión Génica , Regulación hacia Arriba , Western Blotting , Reproducibilidad de los Resultados , Ratas Wistar , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Proteínas Quinasas p38 Activadas por Mitógenos/análisis , Proteínas Quinasas p38 Activadas por Mitógenos/efectos de los fármacos , Diabetes Mellitus Tipo 2/prevención & control , Receptores de Adiponectina/análisis , Receptores de Adiponectina/efectos de los fármacos , Lipoproteína Lipasa/análisis , Lipoproteína Lipasa/efectos de los fármacos
2.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;50(6): e6227, 2017. graf
Artículo en Inglés | LILACS | ID: biblio-839309

RESUMEN

Adiponectin is a multifunctional adipokine that has several oligomeric forms in the blood stream, which broadly regulates innate and acquired immunity. Therefore, in this study, we aimed to observe the differentiation of T helper (Th) cells and expression of costimulatory signaling molecules affected by adiponectin. The mRNA and protein expression levels of adiponectin and its receptors in oxidized low density lipoprotein cholesterol-treated endothelial cells were assayed by real time PCR and immunofluorescence. The endothelial cells were then treated with adiponectin with or without adipoR1 or adipoR2 siRNA and co-cultured with T lymphocytes. The distribution of Th1, Th2 and Th17 subsets were assayed by flow cytometry. The effects of adiponectin on costimulatory signaling molecules HLA-DR, CD80, CD86 and CD 40 was also assayed by flow cytometry. The results showed that endothelial cells expressed adiponectin and its receptor adipoR1 and adipoR2, but not T-cadherin. Adiponectin suppressed Th1 and Th17 differentiation through adipoR1 receptor, contributed to the inhibition of CD80 and CD40, and inhibited differentiation of Th1 and Th17 by inhibiting antigen presenting action.


Asunto(s)
Humanos , Recién Nacido , Adulto , Adiponectina/metabolismo , Antígeno B7-1/metabolismo , Antígenos CD40/metabolismo , Linfocitos T Colaboradores-Inductores/efectos de los fármacos , Adiponectina/genética , Adiponectina/farmacología , Diferenciación Celular , Células Cultivadas , Células Endoteliales/efectos de los fármacos , Células Endoteliales/metabolismo , Antígenos HLA-DR/metabolismo , Células Endoteliales de la Vena Umbilical Humana/citología , Lipoproteínas LDL/farmacología , Receptores de Adiponectina/efectos de los fármacos , Receptores de Adiponectina/metabolismo , Linfocitos T Colaboradores-Inductores/citología , Linfocitos T Colaboradores-Inductores/metabolismo
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