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Biocell
Schisandrin B exerts anticancer effects on human gastric cancer cells through ROS-mediated MAPK, STAT3, and NF-κB pathways
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TIANZHU LI1  YU ZHANG2  TONG ZHANG2  YANNAN LI2  HUI XUE2  JINGLONG CAO2  WENSHUANG HOU2  YINGHUA LUO3  CHENGHAO JIN2 
[1] Department of Molecular Biology, College of Basic Medical Science, Chifeng University;Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Heilongjiang Bayi Agricultural University;Department of Grass Science, College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University;National Coarse Cereals Engineering Research Center
关键词: Schisandrin B;    Gastric cancer;    Reactive oxygen species;    Apoptosis;    Migration;    Cell cycle;   
DOI  :  10.32604/biocell.2023.025593
学科分类:仪器
来源: Biocell
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【 摘 要 】

Schisandrin B (Sch B) is a monomer with anti-cancer and anti-inflammatory effects, which are isolated from theplant Schisandra chinensis (Turcz) Baillon. We investigated the anti-gastric cancer (GC) effects of Sch B and itsunderlying molecular mechanisms. The Cell Counting Kit-8 assay was used to determine the effects of Sch B on theviability of GC and normal cell lines. Hoechst/propidium iodide staining and flow cytometry were used to assess theapoptosis induction of Sch B. Western blotting was used to evaluate the effects of Sch B on downstream apoptoticproteins. The DCFH-DA fluorescent probe was used to assess the regulatory effects of Sch B on reactive oxygenspecies (ROS) levels and related signaling pathways in GC cells. The results showed that Sch B could regulate thephosphorylation level of mitogen-activated protein kinase (MAPK) by upregulating ROS accumulation in gastriccancer cells, and then reduce the expression of nuclear factor kappa B (NF-κB) and phosphorylated transcription3 (p-STAT3). In addition, Sch B downregulated the cell cycle proteins cyclin-dependent kinase 2/4/6 and cyclin D1/E,and arrested cells in the G0/G1 phase. Moreover, it also inhibited cell migration, which was reversed with Nacetylcysteine pretreatment. In summary, Sch B has killing effects on GC cells by upregulating the production ofintracellular ROS and regulating the MAPK/STAT3/NF-κB signaling pathway, leading to the migration arrest andapoptosis of GC cells.

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