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Antitumor effects of pollen polysaccharides from Chinese wolfberry on DU145 cells via the PI3K/AKT pathway in vitro and in vivo

文献类型: 外文期刊

作者: Ran, Linwu 1 ; Chen, Fei 1 ; Zhang, Jing 1 ; Mi, Jia 3 ; Lu, Lu 3 ; Yan, Yamei 3 ; Cao, Youlong 3 ;

作者机构: 1.Ningxia Med Univ, Coll Publ Hlth & Management, Yinchuan 750004, Ningxia, Peoples R China

2.Ningxia Med Univ, Lab Anim Ctr, Yinchuan 750004, Ningxia, Peoples R China

3.Ningxia Acad Agr & Forestry Sci, Inst Wolfberry Engn Technol, Yinchuan 750002, Ningxia, Peoples R China

关键词: Pollen polysaccharides of Chinese wolfberry; DU145 cells; PI3K/AKT pathway

期刊名称:INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES ( 影响因子:6.953; 五年影响因子:6.737 )

ISSN: 0141-8130

年卷期: 2020 年 152 卷

页码:

收录情况: SCI

摘要: Many studies have shown that pollen and its preparation are ideal herbal remedies for the treatment of prostate diseases. Our previous study found that pollen polysaccharides from Chinese wolfberry (WPPs) can induce the apoptosis of prostate cancer DU145 cells. But the antitumor mechanism of WPPs was not clearly understood. Therefore, in the present study, we further investigated the antitumor mechanism of WPPs in DU145 cells and a xenograft mice model. The results showed that WPPs decreased the levels of PI3K, AKT, p-AKT and Bcl-2 proteins, and increased expression of Bax, caspase-3 and caspase-9 in DU145 cells (P < 0.05). The in vivo data demonstrated that WPPs resulted in a significant dose-dependent increase (P < 0.05) in the number of apoptotic cells in tumor tissues. Immunohistochemical analysis showed that the activated PI3K, AKT, p-AKT and Bcl-2 levels were decreased and the level of caspase-3 was increased in DU145 xenografts mice model. Therefore, the antitumor mechanism of WPPs on DU145 cells may involve regulation of the PI3K/AKT signaling pathway, which eventually promotes apoptosis. This study provided the experimental basis for further studied of WPPs as a possible functional food or adjuvant agent for prevention or treatment of prostate cancer. (C) 2019 Published by Elsevier B.V.

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