Hepatocellular carcinoma (HCC) is an aggressive malignancy with high chemoresistance to chemotherapeutics. Arsenic trioxide (ATO) is of therapeutic potential for the treatment of HCC; however, the therapeutic benefit of ATO is very limited due to narrow therapeutic window. Icariin is a natural compound which inhibits tumour cell growth and induces apoptotic cell death in a variety of cancer cells. This study was designed to determine whether Icariin can potentiate the antitumour activity of ATO in HCC treatment. Cell proliferation and apoptosis were measured using an MTT assay and flow cytometry respectively. Changes in reactive oxygen species (ROS) level and mitochondrial membrane potential were analysed by fluorescence signals. Protein expression was measured by western blotting and NF-κB activity was determined by ELISA assay. In addition, the antitumour effect of combination treatment with Icariin and ATO on HCC was evaluated using a murine HCC cancer xenograft model. Icariin inhibited proliferation and induced apoptosis in both of the tested HCC cell lines in a dose-dependent fashion. Icariin enhanced the antitumour activity of ATO both in vitro and in vivo. The antitumour activity of Icariin and its enhancement of the antitumour activity of ATO correlated with the generation of intracellular ROS and inhibition of NF-κB activity. Our results showed that Icariin potentiated the antitumour activity of ATO in HCC. Therefore, we propose that the combination treatment with Icariin and ATO might facilitate the optimization of ATO therapy for patients with HCC.

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This meta-analysis disclosed 2.34 fold increased risk of progressing into steroid-refractory IBD in CMV (+) group compared with the CMV (-) group, indicating that CMV infection might be a plausible cause of steroid-refractory IBD.

Preclinical Research The study evaluated the effect of thalidomide on adhesion molecule expression in acute pancreatitis-associated lung injury in rats. Acute pancreatitis was induced in rats by retrograde infusion of 5% sodium taurocholate into the bile-pancreatic duct, and thalidomide (100 mg/kg) was given daily by intragastric route for 8 days before this treatment. Serum lipase (LPS), protein levels in bronchoalveolar lavage fluid (BALF), superoxide dismutase (SOD), glutathione peroxidase (GSHpx), and malondialdehyde (MDA) levels in lung were measured. Compared with the acute pancreatitis- group, lung histopathology, serum LPS, protein levels in BALF, SOD, GSHpx, and MDA levels, and the expression levels of intercellular adhesion molecule-1 and E-selectin mRNA and protein in rats given thalidomide were improved (P < 0.01). Thus, thalidomide may reduce the expression of adhesion molecules via inhibition of oxidative stress to alleviate acute pancreatitis-associated lung injury in a rat model. Drug Dev Res, 2014. © 2014 Wiley Periodicals, Inc.

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