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        Study on changes and mechanisms of cytokines for alloxan-induced hepatic injury by Cr3+-treatment in mice

        Weijiang Fan,Wenhang Wang,Lan Zhang,Lihong Qi,Anjun Liu,Anjun Liu 대한독성 유전단백체 학회 2016 Molecular & cellular toxicology Vol.12 No.2

        This study investigated the effects of treatment with trivalent chromium (Cr3+) on the cytokine levels in mice that had alloxan-induced hepatic injury. The results showed that chromium picolinate (CrPic) may have a protective effect against hepatic injury and that these effects might be related to changes in cytokine expression. Blood ALT and AST levels in the alloxan mice were higher than those in the control and CrPic-treated groups (no significant differences between the latter groups). Luminex assays of cytokines from Th1 (TNF-α, IL-2 and IL-9) and Th2 (IL-3, IL- 5, IL-6, IL-10, IL-13) - as well as G-CSF, M-CSF, and GM-CSF - demonstrated increased levels of TNF-α, IL-2, and IL-9 (55.10%, 1.05-fold, and 2.14-fold, respectively) in alloxan-treated mice compared to control mice. Further, compared to the control group, liver IL- 3, -5, -6, -10, and -13 levels were decreased 2.45-fold, 1.54-fold, 1.01-fold, 12.6% and 37.3%, respectively, in the alloxan-treated mice. In comparison to the control mice, the levels of G-CSF, M-CSF and GM-CSF were decreased in the alloxan-treated mice (25.2%, 49.5%, and 52.9%, respectively). These cytokines were increased 7.91-fold, 43.67% and 34.05%, respectively, in the CrPic-treated group. These findings suggest that Th1/Th2 type cytokines are involved in hepatic injury and induced by alloxan, which may provide a new possible therapeutic approach through CrPic-treatment.

      • Norcantharidin Anti-Angiogenesis Activity Possibly through an Endothelial Cell Pathway in Human Colorectal Cancer

        Yu, Tao,Hou, Fenggang,Liu, Manman,Zhou, Lihong,Li, Dan,Liu, Jianrong,Fan, Zhongze,Li, Qi Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.2

        The present study was based on the unexpected discovery that norcantharidin exerted anti-angiogenesis activity when effects on growth of human colon cancer were studied. The aim was to further verify this finding and explore possible mechanisms using a tumor xenograft model in nude mice. We confirmed that norcantharidin (5 or 15 mg/kg) could inhibit angiogenesis of human colon cancer in vivo. In vitro, crossing river assay, cell adhesion assay and tube formation assay indicated that NCTD could reduce the migration, adhesion and vascular network tube formation ability of HUVECs. At the same time, the expression levels of VEGF and VEGFR-2 proteins which play important roles in angiogenesis were reduced as examined by western blotting analysis. Taken together, the results firstly showed NCTD could inhibit angiogenesis of human colon cancer in vivo, probably associated with effects on migration, adhesion and vascular network tube formation of HUVECs and expression levels of VEGF and VEGFR-2 proteins.

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