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Down-regulation of IL-6, IL-8, TNF-α and IL-1β by glucosamine in HaCaT cells, but not in the presence of TNF-α

Authors:
Kun Park, Ji-Hye Lee, Ho-Chan Cho, Sun-Young Cho, Jae-We Cho

Affiliations:
Department of Dermatology, College of Medicine Eulji University, Seoul, Korea

Doi:
10.3892/ol_00000051

Pages:
289-292

Abstract:

There is considerable evidence that glucosamine exerts an inhibitory effect on inflammatory cytokine expression in cells. Glucosamine has been recommended as a promising anti-inflammatory modulator, which has been applied in clinical trials for attenuation of the inflammatory process. However, it is unknown whether glucosamine reduces the expression of TNF-α-induced inflammatory cytokines in HaCaT cells. The anti-inflammatory effects of curcumin in HaCaT cells have been extensively investigated in several studies. Thus, in this study we investigated the expression of IL-6, IL-8, TNF-α and IL-1β in glucosamine-treated HaCaT cells, and the effects of glucosamine were compared to those of curcumin-treated HaCaT cells. Our data showed that the expression of IL-6, IL-8, TNF-α and IL-1β was decreased by glucosamine treatment in the HaCaT cells. In contrast, the expression of IL-6, IL-8, TNF-α and IL-1β was not attenuated by glucosamine treatment in the TNF-α-treated HaCaT cells. Notably, curcumin induced an increased expression of IL-8 and IL-1β in the HaCaT cells, but not that of IL-6 and TNF-α. On the other hand, curcumin attenuated the expression of IL-6 and IL-8 in the TNF-α-treated HaCaT cells. Our data indicated that glucosamine induced the down-regulation of IL-6, IL-8, TNF-α and IL-1β expression in the HaCaT cells. However, the stimulation of TNF-α abolished the inhibitory effects of glucosamine on the expression of inflammatory cytokines in the HaCaT cells. Thus, even though glucosamine induces the down-regulation of inflammatory cytokines in HaCaT cells, the anti-inflammatory role of glucosamine in TNF-α-mediated inflammatory skin diseases should be investigated.

Oncology Letters

March-April 2010
Volume 1 Number 2


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