Cytokine levels in acute alcoholic hepatitis: a sequential study

Rodrı́guez-Rodrı́guez, Eva; González‐Reimers, Emilio; Santolaria-Fernández, Francisco; Milena-Abril, Antonio; Rodríguez-Moreno, F.; Oramas-Rodríguez, Juana María; Martı́nez-Riera, Antonio

doi:10.1016/0376-8716(95)01130-q

Cited by 32 publications

(13 citation statements)

References 21 publications

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“…For examples, patients with ALD have several manifestations of the acute phase response, including elevated serum levels of IL-1b and TNF-a [9]. TNF-a levels in patients affected by alcoholic hepatitis are almost significantly higher than in controls, suggesting that enhanced serum levels of TNF-a seem to be related to a worse prognosis in alcoholic hepatitis [22]. Furthermore, ethanol intake increases the serum levels of IL-1b in rats [23].…”

Section: Discussionmentioning

confidence: 97%

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

Hsiang

Cheng

et al. 2005

J Biomed Sci

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Alcoholic liver disease (ALD) is one of the most common liver diseases in the world. Increased levels of proinflammatory cytokines, including interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), have been correlated with the patients affected by ALD. However, the direct effect of alcohol in the induction of IL-1beta and TNF-alpha has not been clarified. In this study, we demonstrated that acetaldehyde, the metabolic product of ethanol, was able to induce IL-1beta and TNF-alpha production in HepG2 cells. Nuclear factor-kappaB (NF-kappaB), the transcription factor involved in the regulation of cytokine production, was also activated by acetaldehyde through inhibitory kappaB-alpha (IkappaB-alpha) phosphorylation and degradation. However, the NF-kappaB inhibitors, such as aspirin, cyclosporin A and dexamethasone, inhibited both the acetaldehyde-induced NF-kappaB activity and the induced cytokine production. Therefore, these data suggested that acetaldehyde stimulated IL-1beta and TNF-alpha production via the regulation of NF-kappaB 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-kappaB activity. Berberine, the major ingredient of these herbs, abolished acetaldehyde-induced NF-kappaB activity and cytokine production in a dose-dependent manner. Moreover, its inhibitory ability was through the inhibition of induced IkappaB-alpha phosphorylation and degradation. In conclusion, we first linked the acetaldehyde-induced NF-kappaB activity to the induced proinflammatory cytokine production in HepG2 cells. Our findings also suggested the potential role of berberine in the treatment of ALD.

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Section: Discussionmentioning

confidence: 97%

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

Hsiang

Cheng

et al. 2005

J Biomed Sci

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“…Increased sTNF-R1 is considered as a naturally occurring substance generated in the course of inflammation to inhibit the biological effects of TNFa, which may be last several weeks [14] in the setting of AH. In this aspect, high serum sTNF-R1 as an independent predictor of short-term mortality suggests the overproduction of this cytokine antagonist is not sufficient to counteract the deleterious effects of TNFa.…”

Section: Discussionmentioning

confidence: 99%

Soluble TNF-R1, but not tumor necrosis factor alpha, predicts the 3-month mortality in patients with alcoholic hepatitis

Spahr

Giostra

Frossard

et al. 2004

Journal of Hepatology

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“…The TNFR1 (p55) receptor is the principal inducer of cytotoxicity, whereas TNFR2 (p75) seems to regulate the binding of TNF-a to TNFR1 (p55). TNFsRp55 is thought to be generated during inflammation, to inhibit the biological effects of TNF-a [32]. TNFsRp55 and TNFsRp75 levels were found to be high in patients with AAH and the plasma concentrations of these molecules were strongly correlated with ballooning, acidophilic bodies, PMN infiltrate, AAH, fibrosis and Maddrey scores, and blood CRP concentration.…”

Section: Adipose Tissue Livermentioning

confidence: 92%

Harmful effect of adipose tissue on liver lesions in patients with alcoholic liver disease

Naveau

Cassard-Doulcier

Njiké-Nakseu

et al. 2010

Journal of Hepatology

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Cytokine levels in acute alcoholic hepatitis: a sequential study

Cited by 32 publications

References 21 publications

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

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

Soluble TNF-R1, but not tumor necrosis factor alpha, predicts the 3-month mortality in patients with alcoholic hepatitis

Harmful effect of adipose tissue on liver lesions in patients with alcoholic liver disease

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