[Signaling pathways in expression of inducible nitric oxide synthase induced by high mobility group box 1 in rat alveolar macrophages].
Zhongguo Yi Xue Ke Xue Yuan Xue Bao
; 28(6): 781-5, 2006 Dec.
Article
en Zh
| MEDLINE
| ID: mdl-17260466
ABSTRACT
OBJECTIVE:
To explore roles of extracellular signal-regulated kinase (ERK) 1/2, p38 mitogen activated protein kinase (p38 MAPK) and nuclear factor (NF) -KB in expression of inducible nitric oxide synthase (iNOS) in rat alveolar macrophages induced by high mobility group box 1 (HMGB1 ).METHODS:
Primary rat alveolar macrophages (PRAMs) cultured in vitro were incubated with PD98059 ( inhibitor against ERK), SB203580 (inhibitor against p38 MAPK) , PDTC (inhibitor against NF-kappaB), or PD98059 plus SB203580 for 2 hours, respectively. HMGB1 was added into the cultures and incubated with cells for 6 hours. Total RNA of PRAMs was extracted and iNOS mRNA expression was semi-quantified with reverse transcription-polymerase chain reaction ( RT-PCR). Greiss reaction was applied to determine nitrite/nitrate (NO2-/NO3- ) concentration in PRAMs culture supernatants.RESULTS:
Expression of iNOS mRNA and NO production in PRAMs culture supernatants were down-regulated by inhibition of ERK or p38 MAPK by PD98059 or SB203580, respectively (P <0. 05). Moreover, inhibition of iNOS expression and NO production was observed after simultaneous pretreatment with PD98059 and SB203580 (P < 0. 05). Expression of iNOS mRNA in PRAMs and NO production in PRAMs culture supernatants were down-regulated by inhibition of NF-kappaB by PDTC (P <0. 05).CONCLUSION:
Cellular signal molecules of ERK, p38 MAPK, and NF-kappaB all participate in the expression of iNOS and NO production in PRAMs induced by HMGB1.
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Bases de datos:
MEDLINE
Asunto principal:
Transducción de Señal
/
Macrófagos Alveolares
/
Quinasas MAP Reguladas por Señal Extracelular
/
Proteínas Quinasas p38 Activadas por Mitógenos
/
Óxido Nítrico Sintasa de Tipo II
Límite:
Animals
Idioma:
Zh
Revista:
Zhongguo Yi Xue Ke Xue Yuan Xue Bao
Año:
2006
Tipo del documento:
Article
País de afiliación:
China