Your browser doesn't support javascript.
loading
Nitric oxide mediated TNF-α, IL-1β gene expression in liver induced by crush injury of rat's soft tissues / 法医学杂志
Journal of Forensic Medicine ; (6): 250-256, 2014.
Artículo en Chino | WPRIM | ID: wpr-983911
ABSTRACT
OBJECTIVE@#To explore the effect of nitric oxide (NO) on the gene expression of hepatic TNF-α and IL-1β by crush injury of rat's soft tissues.@*METHODS@#Rats were randomly divided into sham group, crush group, crush+aminoguanidine (AG) group, and crush+L-arginine (L-Arg) group. Activities of ALT and AST as well as NO level in serum were measured. Gene expressions of TNF-α and IL-1β were detected with RT-PCR.@*RESULTS@#Obvious increase in TNF-α and IL-1β mRNA expression was detected in the crush group compared with the sham group (P<0.05). After pretreated L-Arg, expressions of TNF-α and IL-1β mRNA were markedly increased (P<0.05). After pretreated AG, those indices obviously decreased (P<0.05). Activities of ALT and AST enhanced and NO level increased in the crush group compared with the sham group (P<0.05). Pretreatment with L-Arg or AG led to substantial increased or reduced activities of ALT and AST as well as NO levels, respectively.@*CONCLUSION@#Endogenous NO mediated TNF-α, IL-1β mRNA up expression in liver induced by increased production of NO after crush injury of rat's soft tissues.
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Heridas y Lesiones / ARN Mensajero / Expresión Génica / Factor de Necrosis Tumoral alfa / Interleucina-1beta / Hígado / Óxido Nítrico Límite: Animales Idioma: Chino Revista: Journal of Forensic Medicine Año: 2014 Tipo del documento: Artículo

Similares

MEDLINE

...
LILACS

LIS

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Heridas y Lesiones / ARN Mensajero / Expresión Génica / Factor de Necrosis Tumoral alfa / Interleucina-1beta / Hígado / Óxido Nítrico Límite: Animales Idioma: Chino Revista: Journal of Forensic Medicine Año: 2014 Tipo del documento: Artículo