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        검색결과 2

        1.
        2017.06 KCI 등재 구독 인증기관 무료, 개인회원 유료
        Colorectal cancer is a major cause of morbidity and mortality that accounts for over 9% of all incidences of cancer. Additionally, colorectal cancer is widely recognized as an environmental disease related to ill-defined cultural, social and lifestyle factors including physical activity, obesity, cigarette smoking and heavy alcohol consumption. Accordingly, natural phytochemicals and extracts have attracted attention because of their beneficial biological effects. Coenzyme Q10 (CoQ10) is a common supplementary medicine applied to increase bioenergetic capacity in various diseases. Therefore, in this study, we investigated whether CoQ10 treatment has any inhibitory effects and its related cellular mechanisms in human colon cancer HCT116 cells. A MTT assay revealed that CoQ10 slightly decreased the proliferation of HCT116 cells; however, glutathione- and superoxide dismutase- activity were unchanged in response to CoQ10 treatment. A DCF-DA assay revealed that CoQ10 slightly increased ROS release of HCT116 cells. However, in a nitric oxide (NO) assay, CoQ10 significantly increased NO production in a dose-dependent manner. The results of western blot analysis revealed that the protein levels of Bax, p21 and p53 were increased, whereas the protein level of Bcl2 was decreased suggesting that the CoQ10-mediated inhibitory mechanism is associated with apoptotic signaling. Taken together, our findings indicate that CoQ10 has an inhibitory effect on the growth of colon cancer cells via NO production that is associated with regulation of factors involved in apoptotic signaling including Bax, Bcl2, p21 and p53.
        4,000원
        2.
        2013.09 KCI 등재 구독 인증기관 무료, 개인회원 유료
        Lipopolysaccharide (LPS) is the major of outer membrane of gram-negative bacteria and one of the most potent microbial initiators of inflammation. From the previous study showed that exposure to a low dose of LPS renders animals tolerant to a lethal dose of LPS, and protects against the toxicity of various chemicals. However, the effects of LPS treatment in thioacetamide (TA) - induced liver injury remain largely unknown. Liver injury caused by various toxic chemicals such as carbon tetrachloride, alcohol, dimethylnitrosamine. Here, we induced rat liver injury by intraperitoneal injection of TA, a representative hepatic fibrosis inducer. In this study, we investigated the effects of LPS in TA group, LPS group, LPS/TA group and vehicle control group on Sprague-Dawely rats (five rats for each group). All rats at the end of the experiment were sacrificed, and liver and serum were obtained. Serological analysis and hematoxylin and eosin staining showed that LPS/TA co-treatment was associated with decrease of aspartate aminotransferase (AST), alanine transaminase (ALT) and totalbilirubin and fibrosis than in TA-treated rats. RT-PCR showed that the levels of IL-6 and Cox2 mRNA were lower in the liver of LPS/TA-cotreated rats than in TA-treated rats. There were no significant differences ALT, ALP, AST, total-bilirubin, IL-6 and Cox2 between vehicle control and LPS-treated rats. These results imply that LPS/TA cotreatment partially alleviates the TA-induced liver injury of rats by reducing inflammatory response.
        4,000원