Open Access

ARTICLE

Schisandrin B exerts anticancer effects on human gastric cancer cells through ROS-mediated MAPK, STAT3, and NF-κB pathways

by TIANZHU LI^1,#, YU ZHANG^2,#, TONG ZHANG^2,#, YANNAN LI², HUI XUE², JINGLONG CAO², WENSHUANG HOU², YINGHUA LUO^3,*, CHENGHAO JIN^2,4,*

1 Department of Molecular Biology, College of Basic Medical Science, Chifeng University, Chifeng, 024000, China
2 Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, 163319, China
3 Department of Grass Science, College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing, 163319, China
4 National Coarse Cereals Engineering Research Center, Daqing, 163319, China

* Corresponding Authors: Yinghua Luo, ; Chenghao Jin,
# These authors contributed equally to this work

(This article belongs to the Special Issue: Herbal Active Ingredients: Potential for the Prevention and Treatment of Cancer)

BIOCELL 2023, 47(1), 195-204. https://doi.org/10.32604/biocell.2023.025593

Received 21 July 2022; Accepted 17 August 2022; Issue published 26 September 2022

Abstract

Schisandrin B (Sch B) is a monomer with anti-cancer and anti-inflammatory effects, which are isolated from the plant Schisandra chinensis (Turcz) Baillon. We investigated the anti-gastric cancer (GC) effects of Sch B and its underlying molecular mechanisms. The Cell Counting Kit-8 assay was used to determine the effects of Sch B on the viability of GC and normal cell lines. Hoechst/propidium iodide staining and flow cytometry were used to assess the apoptosis induction of Sch B. Western blotting was used to evaluate the effects of Sch B on downstream apoptotic proteins. The DCFH-DA fluorescent probe was used to assess the regulatory effects of Sch B on reactive oxygen species (ROS) levels and related signaling pathways in GC cells. The results showed that Sch B could regulate the phosphorylation level of mitogen-activated protein kinase (MAPK) by upregulating ROS accumulation in gastric cancer cells, and then reduce the expression of nuclear factor kappa B (NF-κB) and phosphorylated transcription 3 (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 of intracellular ROS and regulating the MAPK/STAT3/NF-κB signaling pathway, leading to the migration arrest and apoptosis of GC cells.

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