Ethyl β-Carboline-3-Carboxylate Increases Cervical Cancer Cell Apoptosis Through ROS-p38 MAPK Signaling Pathway.

Autor:	Sun HN; College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China., Xie DP; College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China., Ren CX; College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China., Guo XY; College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China., Zhang HN; College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China., Xiao WQ; College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China., Han YH; College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China; sunhunan76@163.com., Cui YD; College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China; cuiyudong6@126.com., Kwon T; Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeonbuk, Republic of Korea kwon@kribb.re.kr.
Jazyk:	angličtina
Zdroj:	In vivo (Athens, Greece) [In Vivo] 2022 May-Jun; Vol. 36 (3), pp. 1178-1187.
DOI:	10.21873/invivo.12817
Abstrakt:	Background/aim: Ethyl β-carboline-3-carboxylate (β-CCE) is one of the effective ingredients of Picrasma quassioides (P. quassioides). As a β-carboline alkaloid, it can antagonize the pharmacological effects of benzodiazepines by regulating neurotransmitter secretion through receptors, thus affecting anxiety and physiology. However, its efficacy in cancer treatment is still unclear. Materials and Methods: We explored the effect of b-CCE on SiHa cells using MTT assay, western blot, flow cytometry, LDH release, T-AOC, SOD, and MDA assays. Results: We investigated the cytotoxicity of β-CCE in SiHa cells and verified that β-CCE could induce cell apoptosis in a time- and concentration-dependent manner. In this process, treatment with β-CCE significantly increased the levels of cytoplasmic and mitochondrial reactive oxygen species (ROS), which disturb the oxidation homeostasis by regulating the total antioxidant capacity (T-AOC), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) production. Notably, the addition of N-acetylcysteine (NAC) (ROS scavenger) effectively alleviated β-CCE-induced apoptosis in SiHa cells. In addition, β-CCE might activate the p38/MAPK signaling pathway, as the pre-treatment with SB203580 (p38 inhibitor) significantly reduced β-CCE-induced apoptosis in SiHa cells. Conclusion: β-CCE has an anti-tumor activity. It activates the p38/MAPK signaling pathway by increasing intracellular ROS levels, which subsequently induce SiHa cell apoptosis. Our results provide a novel therapeutic target for treatment of cervical cancer. (Copyright © 2022, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
Databáze:	MEDLINE
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