Acetaldehyde-induced interleukin-1β and tumor necrosis factor-α production is inhibited by berberine through nuclear factor-κB signaling pathway in HepG2 cells

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Title:	Acetaldehyde-induced interleukin-1β and tumor necrosis factor-α production is inhibited by berberine through nuclear factor-κB signaling pathway in HepG2 cells
Authors:	項千芸(Chien-Yun Hsiang);吳世祿(Shih-Lu Wu);鄭欣怡(Shin-Ei Cheng);侯庭鏞(Tin-Yun Ho)*
Contributors:	醫學院醫學系學士班微生物學科
Keywords:	acetaldehyde;alcoholic liver disease;berberine;cytokine;nuclear factor-κB
Date:	2005-10
Issue Date:	2009-08-19 17:23:36 (UTC+8)
Abstract:	Summary Alcoholic liver disease (ALD) is one of the most common liver diseases in the world. Increased levels of proinflammatory cytokines, including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), have been correlated with the patients affected by ALD. However, the direct effect of alcohol in the induction of IL-1β and TNF-α has not been clarified. In this study, we demonstrated that acetaldehyde, the metabolic product of ethanol, was able to induce IL-1β and TNF-α production in HepG2 cells. Nuclear factor-κB (NF-κB), the transcription factor involved in the regulation of cytokine production, was also activated by acetaldehyde through inhibitory κB-α (IκB-α) phosphorylation and degradation. However, the NF-κB inhibitors, such as aspirin, cyclosporin A and dexamethasone, inhibited both the acetaldehyde-induced NF-κB activity and the induced cytokine production. Therefore, these data suggested that acetaldehyde stimulated IL-1β and TNF-α production via the regulation of NF-κB signaling pathway. By screening 297 controlled Chinese medicinal herbs supervised by Committee on Chinese Medicine and Pharmacy at Taiwan, we found that Coptis chinensis (Huang-Lien) and Phellodendron amurense (Huang-Po) were capable of inhibiting acetaldehyde-induced NF-κB activity. Berberine, the major ingredient of these herbs, abolished acetaldehyde-induced NF-κB activity and cytokine production in a dose-dependent manner. Moreover, its inhibitory ability was through the inhibition of induced IκB-α phosphorylation and degradation. In conclusion, we first linked the acetaldehyde-induced NF-κB activity to the induced proinflammatory cytokine production in HepG2 cells. Our findings also suggested the potential role of berberine in the treatment of ALD.
Relation:	JOURNAL OF BIOMEDICAL SCIENCE 12(5):791~801
Appears in Collections:	[School of Medicine] Journal articles

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