KMID : 0383820100680030168
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Tuberculosis and Respiratory Diseases 2010 Volume.68 No. 3 p.168 ~ p.174
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Role of Insulin in the Activation of NF-¥êB/I¥êB Pathway in Macrophage Cells
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Lee Sang-Min
Jang Yeon-Sil Lee Choon-Taek Kim Young-Whan Han Sung-Koo Shim Young-Soo Yoo Chul-Gyu
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Abstract
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Background: Sepsis still has a high mortality rate despite adequate supportive care. Newer therapeutic modalities have been developed but they have generally ended in failure. Recently, insulin was reported to have an anti- inflammatory effect by inhibiting the I¥êB/NF-¥êB pathway, and may have therapeutic potential in sepsis. However, the precise mechanism of the anti-inflammatory effect of insulin is unclear. This study examined the role of insulin in activating I¥êB/NF-¥êB in macrophage.
Materials and Methods: Raw 264.7 cells, a murine macrophage cell line, were used in this experiment. Western blotting using I¥êB Ab and phosphor-specific I¥êB Ab was performed to evaluate the degradation and phosphorylation of I¥êB cells. For the I¥êB Kinase (IKK) activity, an immune complex kinase assay was performed. The level of interleukin-6 (IL-6) was measured by ELISA to determine the level of proinflammatory cytokine.
Results: I¥êB¥á degradation began 30 min after lipopolysaccharide (LPS) treatment. However, an insulin pretreatment suppressed the I¥êB¥á degradation caused by the LPS treatment. The phosphorylation of I¥êB¥á and IKK activity was also inhibited by the insulin pretreatment. Finally, the insulin pretreatment showed a tendency to suppress the induction of IL-6 by LPS.
Conclusion: Insulin might have an anti-inflammatory effect though partial inhibition of the I¥êB/NF¥êB pathway in macrophage cell lines.
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KEYWORD
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Insulin, Sepsis, Inflammation, NF¥êB
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