激酶
ASK1
生物
癌症研究
蛋白激酶A
细胞生物学
p38丝裂原活化蛋白激酶
MAP激酶激酶激酶
丝裂原活化蛋白激酶激酶
丝裂原活化蛋白激酶
信号转导
分子生物学
作者
Abedul Haque,Naoki Koide,Imtiaz Iftakhar-E-Khuda,Abu Shadat Mohammod Noman,Erdenezaya Odkhuu,Battuvshin Badamtseren,Yoshikazu Naiki,Takayuki Komatsu,Tomoaki Yoshida,Takashi Yokochi
标识
DOI:10.1111/j.1348-0421.2010.00304.x
摘要
Flavopiridol is a cyclin-dependent kinase inhibitor and inhibits the growth of various cancer cells. The effect of flavopiridol on lipopolysaccharide (LPS)-induced proinflammatory mediator production was examined in RAW 264.7 macrophage-like cells. Flavopiridol significantly reduced the production of tumor necrosis factor-α and, to a lesser extent, nitric oxide in LPS-stimulated cells. Flavopiridol inhibited the activation of nuclear factor-κB and IκB kinase in response to LPS. Flavopiridol also inhibited the activation of a series of mitogen-activated protein kinases, such as p38, stress-activated protein kinase/c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2 in response to LPS. However, flavopiridol did not alter the expression of tumor necrosis factor receptor-associated factor 6, myeloid differentiation factor 88 (MyD88) or CD14/toll-like receptor (TLR) 4. Flavopiridol inhibited nitric oxide production induced by a MyD88-dependent TLR2 ligand, but not a MyD88-independent TLR3 ligand. Further, flavopiridol did not alter the phosphorylation of interferon regulatory factor 3 in the MyD88-independent pathway. Therefore, it was suggested that flavopiridol exclusively inhibited the activation of nuclear factor-κB and mitogen-activated protein kinases in the MyD88-dependent pathway. Flavopiridol might be useful for the prevention of LPS-induced inflammatory response.
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