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Objective: To discover the expression pattern and potential underlying mechanism of the caspase recruitment domain‐containing protein 9 (CARD9) in oral squamous cell carcinoma (OSCC). Methods: Caspase recruitment domain‐containing protein 9 expression was detected by qRT‐PCR and Western blot in OSCC tissues and cells, and OSCC (CGHNC9 and OECM‐1) cell lines were divided into control, NC siRNA, and CARD9 siRNA groups. Then, MTT, flow cytometry, wound‐healing, and Transwell assays were carried out to determine the changes in cellular biological characteristics. Immunoblot assay was performed for the expressions of NF‐κB pathway. Finally, we constructed the xenograft models in nude mice to validate the in vivo effect of CARD9 siRNA on OSCC cell growth. Results: Caspase recruitment domain‐containing protein 9 was upregulated in both OSCC tissues and cells, exhibiting a close relation with major clinicopathological features of OSCC patients. Transfection of CARD9 siRNA inhibited the proliferation, migration, and invasion of OSCC cells with the enhanced cell apoptosis, and meanwhile, CARD9, p‐p65/p65, p‐IKKα/IKKα, and p‐IkBα/IkBα were downregulated. The tumor formation assay on nude mice also suggested that CARD9 siRNA might block the in vivo growth of OSCC cells. Conclusion: Caspase recruitment domain‐containing protein 9 suppression results in the upregulation of NF‐κB pathway with suppressed proliferation, migration, and invasion of OSCC cells and facilitates the apoptosis. [ABSTRACT FROM AUTHOR]

A hepatitis B virus (HBV) transgenic mice model was used to establish the fatty liver superimposed model by feeding the methionine choline-deficient (MCD) diet for 8 weeks, with or without the gavage of 2 mg/kg zeaxanthin dipalmitate (ZD) three times per week. Both wild-type and HBV transgenic mice, with MCD diet, gained typical non-obese non-alcoholic steatohepatitis (NASH) and HBV symptoms. Coadministration with ZD exhibited evident therapeutic effects through alleviating those pathological events. Moreover, long-term vehicle-ZD treatment was found to be safe. Thus, ZD is a promising and safe hepato-protective agent against hepatic injury induced by superimposed HBV and NASH in non-obese mice. [ABSTRACT FROM AUTHOR]

Purpose: To study the protective effects and underlying molecular mechanisms of SAMC on carbon tetrachloride (CCl)-induced acute hepatotoxicity in the mouse model. Methods: Mice were intraperitoneally injected with CCl (50 μl/kg; single dose) to induce acute hepatotoxicity with or without a 2-h pre-treatment of SAMC intraperitoneal injection (200 mg/kg; single dose). After 8 h, the blood serum and liver samples of mice were collected and subjected to measurements of histological and molecular parameters of hepatotoxicity. Results: SAMC reduced CCl-triggered cellular necrosis and inflammation in the liver under histological analysis. Since co-treatment of SAMC and CCl enhanced the expressions of antioxidant enzymes, reduced the nitric oxide (NO)-dependent oxidative stress, and inhibited lipid peroxidation induced by CCl. SAMC played an essential antioxidative role during CCl-induced hepatotoxicity. Administration of SAMC also ameliorated hepatic inflammation induced by CCl via inhibiting the activity of NF-κB subunits p50 and p65, thus reducing the expressions of pro-inflammatory cytokines, mediators, and chemokines, as well as promoting pro-regenerative factors at both transcriptional and translational levels. Conclusions: Our results indicate that SAMC mitigates cellular damage, oxidative stress, and inflammation in CCl-induced acute hepatotoxicity mouse model through regulation of NF-κB. Garlic or garlic derivatives may therefore be a potential food supplement in the prevention of liver damage. [ABSTRACT FROM AUTHOR]