Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Ginsenoside induces apoptosis, autophagy and cell cycle arrest in gastric cancer cells by regulation of reactive oxygen species and activation of MAPK pathway

Jingfen Lu¹, Lin Yang¹, Qicong Zhu¹ , Peng Gao², Zhengyi Zhang¹, Wei Wang³

¹Department of Oncology, The 928th Hospital of the Joint Logistic Support Force of the People's Liberation Army, Haikou 570100, Hainan Province, China; ²Department of Gastroesophageal, Hainan Cancer Hospital, Haikou 570100, Hainan Province, China; ³Department of General Surgery, The Fourth People's Hospital of Haikou City, Haikou 570100, Hainan Province, China.

For correspondence:- Qicong Zhu Email: zhuqicong1565@163.com

Accepted: 26 September 2022 Published: 28 October 2022

Citation: Lu J, Yang L, Zhu Q, Gao P, Zhang Z, Wang W. Ginsenoside induces apoptosis, autophagy and cell cycle arrest in gastric cancer cells by regulation of reactive oxygen species and activation of MAPK pathway. Trop J Pharm Res 2022; 21(10):2071-2076 doi: 10.4314/tjpr.v21i10.5

© 2022 The authors.
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Abstract

Purpose: To study the influence of ginsenoside on apoptosis, cell cycle and autophagy in gastric carcinoma (GC), and its effect on reactive oxygen species (ROS) levels and the mitogen-activated protein kinase (MAPK) pathway.

Methods: Human gastric cancer cell line BGC-823 was randomly divided into the following groups: control, 100 μM ginsenoside (Rg5), 150 μM Rg5, and 200 μM Rg5 groups. Western blot assay was used to determine the expressions of autophagy-associated protein 12 (Atg12), Beclin-1, lc3b II, cycle-related protein, phosphated mitotic cyclin 25 homologous protein C (p-cdc25c), cyclin B1, and MAPK signaling pathway-related proteins.

Results: There was significantly higher apoptosis in Rg5-treated BGC-823 cells than in untreated cells. Relative protein levels of Beclin-1, Atg5, Atg12, and lc3b II in BGC-823 cells in Rg5 groups were significantly and concentration-dependently up-regulated, relative to the corresponding expression levels in untreated cells. There were markedly up-regulated proteins of p-cdc25c, cyclin B1 and p-cdc2 in Rg5-exposed BGC-823 cells than in untreated cells, while CDC2 protein expression was significantly and concentration-dependently lower than that of control group (p < 0.05). Rg5 treatment resulted in marked and concentration-dependent increases in ROS levels in BGC-823 cells, relative to control cells (p < 0.05), whereas the expression levels of p-p38, p-JNK and p-ERK were significantly higher in Rg5-exposed cells than in unexposed cells (p < 0.05).

Conclusion: Ginsenoside induces apoptosis, autophagy and cycle interruption in GC cells by regulating ROS production and activating MAPK pathway. Therefore, ginsenoside may be a promising agent for the management of gastric cancer. However, there is a need to conduct in vivo studies on the compound.

Keywords: Ginsenoside, Reactive active species, MAPK, Autophagy, Protein expressions