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  • Open Access

    ARTICLE

    Oleanolic acid inhibits colon cancer cell stemness and reverses chemoresistance by suppressing JAK2/STAT3 signaling pathway

    RUOYU CHEN1, YIMAN WU1, FENG WANG1, JUNTAO ZHOU1, HUAZHANG ZHUANG1, WEI LI2,*

    BIOCELL, Vol.48, No.7, pp. 1037-1046, 2024, DOI:10.32604/biocell.2024.051074

    Abstract Background: Oleanolic acid (OA), a pentacyclic triterpenoid exhibiting specific anti-cancer properties and highly effective antioxidant activity, was isolated from traditional Chinese medicinal herbs. Conversely, the OA that impacts colon cancer (CC) cells and its underlying mechanisms remain poorly understood. Methods: The cytotoxic effect of OA alone or OA-5-Fluorouracil (5-FU) combination on normal and CC cells was analyzed by methyl thiazolyl diphenyl-tetrazolium bromide (MTT). Then, the impact of OA on CC cell lines (LoVo and HT-29) proliferation and stemness were measured using colon formation and tumorsphere formation assays. Octamer-binding transcription factor 4 (Oct4), Prominin-1 (CD133), Nanog,… More >

  • Open Access

    ARTICLE

    Protective effects of docosahexaenoic acid against non-alcoholic hepatic steatosis through activating of JAK2/STAT3 signaling pathway

    YUE WANG1,#, YINPING DUAN1,#, KUNLIN CHEN3, HUIXIA LI1,2,*, YAN QUAN4,*

    BIOCELL, Vol.45, No.2, pp. 307-316, 2021, DOI:10.32604/biocell.2021.014305

    Abstract Non-alcoholic fatty liver disease is the most common cause of hepatic dysfunction. In the present study, human normal hepatocyte L02 cells were treated with 50% fetal bovine serum to induce the formation of hepatic steatosis in vitro, and then the cells were treated with docosahexaenoic acid to investigate its protective effect on Non-alcoholic fatty liver disease. Our results showed that 50% of fetal bovine serum significantly induced intracellular lipid accumulation and hepatocyte fatty degeneration within 48 h. The expression level of adipose formation-related genes was significantly up-regulated, such as PPARγ, C/EBPα and SREBP-1; meanwhile, the content… More >

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