Plasma iPGE2 and i6-keto PGF1α in the course of liver cirrhosis

Flisiak, Robert; Prokopowicz, D

doi:10.1016/s0090-6980(96)00137-2

Cited by 16 publications

(5 citation statements)

References 25 publications

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“…For example, PGE2 delays collagen formation and up-regulates tissue inhibitor of metalloproteinases-2 leading to matrix accumulation in rat liver [21]. It has been shown that plasma levels of PGE2 increase with the advancement of liver cirrhosis [22]. COX-2 expression has not been described previously in relation with HBV protein.…”

Section: Discussionmentioning

confidence: 96%

Recombinant HBsAg inhibits LPS-induced COX-2 expression and IL-18 production by interfering with the NFκB pathway in a human monocytic cell line, THP-1

Cheng

Imanishi

Morisaki

et al. 2005

Journal of Hepatology

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Section: Discussionmentioning

confidence: 96%

Recombinant HBsAg inhibits LPS-induced COX-2 expression and IL-18 production by interfering with the NFκB pathway in a human monocytic cell line, THP-1

Cheng

Imanishi

Morisaki

et al. 2005

Journal of Hepatology

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“…Therefore, the possible reason for an elevated plasma TGF-β 1 in patients with chronic liver diseases is enhanced intercellular signalling related to inflammation and fibrotic activity in the liver. Some other bioactive substances involved in this process, such as prostanoids, have previously been evaluated as possible prognostic markers of liver cirrhosis development (6). TGF-β 1 is the most abundant isoform of TGF in both normal and fibrotic liver (8).…”

Section: Discussionmentioning

confidence: 99%

“…Results were analysed with respect to aetiology and the degree of liver insufficiency as evaluated by the Child-Pugh classification (5). The presence of ascites and/or encephalopathy, the prothrombin index, as well as concentrations of bilirubin and albumin were recorded for this purpose and patients' liver dysfunction was scored as previously described (6). Additionally, biochemical indices of hepatocyte injury (alanine and aspartate aminotransferases) and cholestasis (alkaline phosphatase, γ-glutamyl transpeptidase) were analysed.…”

Section: Patients Materials and Methodsmentioning

confidence: 99%

Transforming Growth Factor-β1 as a Surrogate Marker of Hepatic Dysfunction in Chronic Liver Diseases

Flisiak

Prokopowicz²

2000

Clinical Chemistry and Laboratory Medicine

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The aim of the study was to evaluate the possible association between plasma concentrations of transforming growth factor-beta1 (TGF-beta1) and the degree of hepatic dysfunction in patients with chronic liver diseases. TGF-beta1 was measured with an enzyme immunoassay in plasma from 21 patients with chronic active hepatitis and 40 patients with liver cirrhosis. Normal values were obtained from a group of 13 healthy volunteers. Results were analysed with respect to aetiology and the degree of liver insufficiency as evaluated by the Child-Pugh classification. The mean plasma concentration of TGF-beta1 in patients (36.9+/-2.8 ng/ml) was twice that found in normal volunteers (18.3+/-1.6 ng/ml). The highest values were observed in patients with alcoholic liver cirrhosis (44.4+/-4.7 ng/ml). Plasma TGF-beta1 showed a statistically significant positive correlation with the degree of liver insufficiency. These results indicate the possible use of plasma TGF-beta1 measurement as a good marker of liver function impairment. Further observation of patients involved in this study may help to evaluate its possible prognostic value in chronic liver diseases.

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“…Various studies have shown increased production of the COX products from chronically injured livers in both animal and human models (7,10,11,22,26,28,44,46,47). Increased levels of TXA 2 have been reported in the systemic circulation after bile duct ligation (BDL)-induced cirrhosis (15).…”

mentioning

confidence: 99%

Role of thromboxane A₂in early BDL-induced portal hypertension

Yokoyama

Kresge

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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Although the mechanisms of cirrhosis-induced portal hypertension have been studied extensively, the role of thromboxane A2 (TXA2) in the development of portal hypertension has never been explicitly explored. In the present study, we sought to determine the role of TXA2 in bile duct ligation (BDL)-induced portal hypertension in Sprague-Dawley rats. After 1 wk of BDL or sham operation, the liver was isolated and perfused with Krebs-Henseleit bicarbonate buffer at a constant flow rate. After 30 min of nonrecirculating perfusion, the buffer was recirculated in a total volume of 100 ml. The perfusate was sampled for the enzyme immunoassay of thromboxane B2(TXB2), the stable metabolite of TXA2. Although recirculation of the buffer caused no significant change in sham-operated rats, it resulted in a marked increase in portal pressure in BDL rats. The increase in portal pressure was found concomitantly with a significant increase of TXB2 in the perfusate (sham vs. BDL after 30 min of recirculating perfusion: 1,420 ± 803 vs. 10,210 ± 2,950 pg/ml; P < 0.05). Perfusion with a buffer containing indomethacin or gadolinium chloride for inhibition of cyclooxygenase (COX) or Kupffer cells, respectively, substantially blocked the recirculation-induced increases in both portal pressure and TXB2 release in BDL group. Hepatic detection of COX gene expression by RT-PCR revealed that COX-2 but not COX-1 was upregulated following BDL, and this upregulation was confirmed at the protein level by Western blot analysis. In conclusion, these results clearly demonstrate that increased hepatic TXA2 release into the portal circulation contributes to the increased portal resistance in BDL-induced liver injury, suggesting a role of TXA2 in liver fibrosis-induced portal hypertension. Furthermore, the Kupffer cell is likely the source of increased TXA2, which is associated with upregulation of the COX-2 enzyme.

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Plasma iPGE2 and i6-keto PGF1α in the course of liver cirrhosis

Cited by 16 publications

References 25 publications

Recombinant HBsAg inhibits LPS-induced COX-2 expression and IL-18 production by interfering with the NFκB pathway in a human monocytic cell line, THP-1

Recombinant HBsAg inhibits LPS-induced COX-2 expression and IL-18 production by interfering with the NFκB pathway in a human monocytic cell line, THP-1

Transforming Growth Factor-β1 as a Surrogate Marker of Hepatic Dysfunction in Chronic Liver Diseases

Role of thromboxane A₂in early BDL-induced portal hypertension

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Plasma iPGE2 and i6-keto PGF1α in the course of liver cirrhosis

Cited by 16 publications

References 25 publications

Recombinant HBsAg inhibits LPS-induced COX-2 expression and IL-18 production by interfering with the NFκB pathway in a human monocytic cell line, THP-1

Recombinant HBsAg inhibits LPS-induced COX-2 expression and IL-18 production by interfering with the NFκB pathway in a human monocytic cell line, THP-1

Transforming Growth Factor-β1 as a Surrogate Marker of Hepatic Dysfunction in Chronic Liver Diseases

Role of thromboxane A2in early BDL-induced portal hypertension

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Role of thromboxane A₂in early BDL-induced portal hypertension