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Arginine Supplementation Induces Arginase Activity and Inhibits TNF-α Synthesis in Mice Spleen Macrophages After Intestinal Obstruction.
Quirino, Iara Eliza Pacífico; Carneiro, Matheus Batista Heitor; Cardoso, Valbert Nascimento; das Graças Carvalho Dos Santos, Rosana; Vieira, Leda Quercia; Fiuza, Jacqueline Araújo; Alvarez-Leite, Jacqueline Isaura; de Vasconcelos Generoso, Simone; Correia, Maria Isabel.
Afiliación
  • Quirino IE; Department of Clinical Analysis and Toxicology, Pharmacy School, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
  • Carneiro MB; Department of Biochemistry and Immunology, Biologic Sciences Institute, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
  • Cardoso VN; Department of Clinical Analysis and Toxicology, Pharmacy School, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
  • das Graças Carvalho Dos Santos R; Department of Clinical Analysis and Toxicology, Pharmacy School, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
  • Vieira LQ; Department of Biochemistry and Immunology, Biologic Sciences Institute, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
  • Fiuza JA; Renè Rachou Research Center, Fundação Oswaldo Cruz, Belo Horizonte, MG, Brazil Department of Parasitology, Biologic Sciences Institute Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
  • Alvarez-Leite JI; Department of Biochemistry and Immunology, Biologic Sciences Institute, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
  • de Vasconcelos Generoso S; Department of Nutrition, Nursing School, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil simonenutufmg@gmail.com.
  • Correia MI; Department of Surgery, Medical School, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
JPEN J Parenter Enteral Nutr ; 40(3): 417-22, 2016 Mar.
Article en En | MEDLINE | ID: mdl-25135690
BACKGROUND: The purpose of this study was to assess the effect of arginine supplementation on arginase activity, tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) synthesis in cultured splenic macrophages from a murine model of intestinal obstruction (IO). The effects of nitric oxide synthase (iNOS) inhibition were also studied using iNOS knockout animals. MATERIAL AND METHODS: Male C57BL6/J wild-type (WT) and iNOS knockout (iNOS-/-) mice were randomized into 6 groups: Sham and Sham-/- (standard chow), IO and IO-/- (standard chow + IO), and Arg and Arg-/- (standard chow supplemented with arginine + IO). After 7 days of treatment with standard or supplemented chow, IO was induced. Arginase activity as well as TNF-α and IL-10 levels were analyzed in splenic macrophage cultures. RESULTS: Arginine supplementation and the absence of iNOS increased arginase activity in splenic macrophages (Arg, IO-/-, and Arg-/- groups vs the Sham group; P < .05). Arginine was also related to a decrease in TNF-α levels (Arg vs IO group, P < .05) and maintenance of IL-10 levels (Arg vs other groups, P > .05). The inhibition of iNOS did not result in effects on the concentration of cytokines (Sham-/-, IO-/-, and Arg-/- vs other, P < .05). CONCLUSIONS: Arginine supplementation and iNOS inhibition led to increased arginase activity. Arginine availability decreased plasma TNF-α levels, which may be directly related to nitric oxide derived from arginine.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Arginasa / Arginina / Bazo / Factor de Necrosis Tumoral alfa / Obstrucción Intestinal / Macrófagos Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: JPEN J Parenter Enteral Nutr Año: 2016 Tipo del documento: Article País de afiliación: Brasil Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Arginasa / Arginina / Bazo / Factor de Necrosis Tumoral alfa / Obstrucción Intestinal / Macrófagos Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: JPEN J Parenter Enteral Nutr Año: 2016 Tipo del documento: Article País de afiliación: Brasil Pais de publicación: Estados Unidos