Adiponectin modulates DCA-induced inflammation via the ROS/NF-κ B signaling pathway in esophageal adenocarcinoma cells.

BACKGROUND: Deoxycholic acid (DCA) promotes the development and progression of esophageal adenocarcinoma (EAC) by inducing inflammation. Adiponectin is reported to have anti-inflammatory and anti-tumor effects. PURPOSE: This study investigated the effects of two types of adiponectin, full-length adiponectin (f-Ad) and globular adiponectin (g-Ad), on DCA-induced inflammation, and investigated the involvement of the reactive oxygen species (ROS)/NF-κB signaling pathway in inflammation in EAC. METHODS: OE19 cells were treated with DCA (50-300 µM) and/or f-Ad/g-Ad (10.0 µg/ml) or N-acetylcysteine (NAC). The viability of cells exposed to DCA was measured by use of the MTT assay. mRNA and protein levels of the inflammatory factors were examined by real-time PCR and ELISA. Intra-cellular ROS levels were determined by use of flow cytometry. Protein levels of total and p-NF-κB p65 were measured by western blot. RESULTS: DCA induced dose and time-dependent cytotoxicity. mRNA and protein expression of TNF-α, IL-8, and IL-6 in cells treated with DCA alone were up-regulated, and intra-cellular ROS and p-NF-κB p65 protein levels were also increased. g-Ad promoted inflammatory factor production, ROS levels, and p-NF-κB p65 protein expression whereas f-Ad had a suppressive effect. When combined with DCA, g-Ad enhanced the pro-inflammatory effect of DCA whereas f-Ad, similar to NAC, suppressed the effect. CONCLUSION: DCA has a pro-inflammatory effect in EAC. f-Ad has an anti-inflammatory effect whereas g-Ad seems to have a pro-inflammatory effect in an ROS/NF-κB p65-dependent manner. This indicates that f-Ad could be a potential anti-inflammatory reagent for cancer therapy.

The role of intravascular intervention in the management of Budd-Chiari syndrome.

OBJECTIVE: To evaluate the efficacy of intravascular intervention in the management of different types of Budd-Chiari syndrome. METHODS: Fifty-three patients of BCS were clinically diagnosed and interventionally treated in terms of their signs and symptoms of portal hypertension and occlusive inferior vena cava/or hepatic veins with the combination of Doppler ultrasonography, CT scan, and angiography. The interventional methods applied in this study included percutaneous transluminal angioplasty and IVC stent implantation (PTA+IVC stent); transjugular hepatic veno-stent placement (PTA+HV stent) or transjugular transluminal hepatic veno-inferior vena cava stent placement and transcaval transjugular intrahepatic portocaval shunt. RESULTS: The success rate of intravascular interventional therapy was 92.45% (49/53). After interventional therapy, the patients' pleural effusion, ascites, prominent veins formation of bilateral flanks or backs alleviated, hepatomegaly reduced, and the urinary output increased. The longest follow-up case was 13 years with patent stent. Two patients died of pulmonary embolization or pericardial tamponade during surgery. CONCLUSION: Intravascular intervention is a safe and effective therapy for most types of BCS.