Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction

Detalhes bibliográficos
Autor(a) principal: Lv, Dan
Data de Publicação: 2020
Outros Autores: Pan, Li-hong, Zhang, Ren, Yang, Jie, Chen, Hao, Wen, Yanzhang, Huang, Mi, Ma , Xinhua, Wang, Qiang, Yang, Xinzhou
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Brazilian Journal of Pharmaceutical Sciences
Texto Completo: https://www.revistas.usp.br/bjps/article/view/181352
Resumo: Hepatocellular carcinoma is one of the most prevalent malignancies and a leading cause of cancer-related mortality worldwide. However, the therapies to prevent hepatocellular carcinoma are still limited and the emergence of drug resistance leads to the development of new anti-cancer drugs and combinational chemotherapy regimens. Our study was aimed to explore the anticancer effects of the essential oil extract (EEEO) from Euphorbia esula which has been widely used in traditional Chinese folk medicine and possessed potential cytotoxic effects in several human tumor cells. However, the mechanisms of EEEOinduced anti-proliferation and apoptosis have not been completely elucidated. In this study, EEEO was prepared by hydro-distillation and the main chemical component of EEEO was identified by GC-MS. HepG2 cells were treated with EEEO in vitro and then evaluated with respect to proliferation, apoptosis, and levels of reactive oxygen species (ROS) and apoptotic proteins. Our studies showed that EEEO decreased cell viability, elevated ROS levels, and induced apoptosis of HepG2 cells in a concentrationand time-dependent manner. Furthermore, Bcl-2 was down-regulated, while Bax was up-regulated in HepG2 after EEEO treatment. These results suggest that EEEO induced apoptosis of HepG2 cells and indicate that this apoptosis might be mediated by the mitochondrial pathway.
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spelling Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunctionEuphorbia esulaHepatocellular carcinomaApoptosisReactive oxygen speciesMitochondrial pathwayHepatocellular carcinoma is one of the most prevalent malignancies and a leading cause of cancer-related mortality worldwide. However, the therapies to prevent hepatocellular carcinoma are still limited and the emergence of drug resistance leads to the development of new anti-cancer drugs and combinational chemotherapy regimens. Our study was aimed to explore the anticancer effects of the essential oil extract (EEEO) from Euphorbia esula which has been widely used in traditional Chinese folk medicine and possessed potential cytotoxic effects in several human tumor cells. However, the mechanisms of EEEOinduced anti-proliferation and apoptosis have not been completely elucidated. In this study, EEEO was prepared by hydro-distillation and the main chemical component of EEEO was identified by GC-MS. HepG2 cells were treated with EEEO in vitro and then evaluated with respect to proliferation, apoptosis, and levels of reactive oxygen species (ROS) and apoptotic proteins. Our studies showed that EEEO decreased cell viability, elevated ROS levels, and induced apoptosis of HepG2 cells in a concentrationand time-dependent manner. Furthermore, Bcl-2 was down-regulated, while Bax was up-regulated in HepG2 after EEEO treatment. These results suggest that EEEO induced apoptosis of HepG2 cells and indicate that this apoptosis might be mediated by the mitochondrial pathway.Universidade de São Paulo. Faculdade de Ciências Farmacêuticas2020-12-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/bjps/article/view/18135210.1590/s2175-97902019000317542Brazilian Journal of Pharmaceutical Sciences; Vol. 56 (2020); e17542Brazilian Journal of Pharmaceutical Sciences; v. 56 (2020); e17542Brazilian Journal of Pharmaceutical Sciences; Vol. 56 (2020); e175422175-97901984-8250reponame:Brazilian Journal of Pharmaceutical Sciencesinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/bjps/article/view/181352/168239Copyright (c) 2020 Brazilian Journal of Pharmaceutical Scienceshttp://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessLv, Dan Pan, Li-hong Zhang, Ren Yang, Jie Chen, Hao Wen, Yanzhang Huang, Mi Ma , Xinhua Wang, Qiang Yang, Xinzhou 2021-06-12T19:46:54Zoai:revistas.usp.br:article/181352Revistahttps://www.revistas.usp.br/bjps/indexPUBhttps://old.scielo.br/oai/scielo-oai.phpbjps@usp.br||elizabeth.igne@gmail.com2175-97901984-8250opendoar:2021-06-12T19:46:54Brazilian Journal of Pharmaceutical Sciences - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction
title Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction
spellingShingle Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction
Lv, Dan
Euphorbia esula
Hepatocellular carcinoma
Apoptosis
Reactive oxygen species
Mitochondrial pathway
title_short Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction
title_full Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction
title_fullStr Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction
title_full_unstemmed Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction
title_sort Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction
author Lv, Dan
author_facet Lv, Dan
Pan, Li-hong
Zhang, Ren
Yang, Jie
Chen, Hao
Wen, Yanzhang
Huang, Mi
Ma , Xinhua
Wang, Qiang
Yang, Xinzhou
author_role author
author2 Pan, Li-hong
Zhang, Ren
Yang, Jie
Chen, Hao
Wen, Yanzhang
Huang, Mi
Ma , Xinhua
Wang, Qiang
Yang, Xinzhou
author2_role author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Lv, Dan
Pan, Li-hong
Zhang, Ren
Yang, Jie
Chen, Hao
Wen, Yanzhang
Huang, Mi
Ma , Xinhua
Wang, Qiang
Yang, Xinzhou
dc.subject.por.fl_str_mv Euphorbia esula
Hepatocellular carcinoma
Apoptosis
Reactive oxygen species
Mitochondrial pathway
topic Euphorbia esula
Hepatocellular carcinoma
Apoptosis
Reactive oxygen species
Mitochondrial pathway
description Hepatocellular carcinoma is one of the most prevalent malignancies and a leading cause of cancer-related mortality worldwide. However, the therapies to prevent hepatocellular carcinoma are still limited and the emergence of drug resistance leads to the development of new anti-cancer drugs and combinational chemotherapy regimens. Our study was aimed to explore the anticancer effects of the essential oil extract (EEEO) from Euphorbia esula which has been widely used in traditional Chinese folk medicine and possessed potential cytotoxic effects in several human tumor cells. However, the mechanisms of EEEOinduced anti-proliferation and apoptosis have not been completely elucidated. In this study, EEEO was prepared by hydro-distillation and the main chemical component of EEEO was identified by GC-MS. HepG2 cells were treated with EEEO in vitro and then evaluated with respect to proliferation, apoptosis, and levels of reactive oxygen species (ROS) and apoptotic proteins. Our studies showed that EEEO decreased cell viability, elevated ROS levels, and induced apoptosis of HepG2 cells in a concentrationand time-dependent manner. Furthermore, Bcl-2 was down-regulated, while Bax was up-regulated in HepG2 after EEEO treatment. These results suggest that EEEO induced apoptosis of HepG2 cells and indicate that this apoptosis might be mediated by the mitochondrial pathway.
publishDate 2020
dc.date.none.fl_str_mv 2020-12-09
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/bjps/article/view/181352
10.1590/s2175-97902019000317542
url https://www.revistas.usp.br/bjps/article/view/181352
identifier_str_mv 10.1590/s2175-97902019000317542
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/bjps/article/view/181352/168239
dc.rights.driver.fl_str_mv Copyright (c) 2020 Brazilian Journal of Pharmaceutical Sciences
http://creativecommons.org/licenses/by/4.0
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2020 Brazilian Journal of Pharmaceutical Sciences
http://creativecommons.org/licenses/by/4.0
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Universidade de São Paulo. Faculdade de Ciências Farmacêuticas
publisher.none.fl_str_mv Universidade de São Paulo. Faculdade de Ciências Farmacêuticas
dc.source.none.fl_str_mv Brazilian Journal of Pharmaceutical Sciences; Vol. 56 (2020); e17542
Brazilian Journal of Pharmaceutical Sciences; v. 56 (2020); e17542
Brazilian Journal of Pharmaceutical Sciences; Vol. 56 (2020); e17542
2175-9790
1984-8250
reponame:Brazilian Journal of Pharmaceutical Sciences
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Brazilian Journal of Pharmaceutical Sciences
collection Brazilian Journal of Pharmaceutical Sciences
repository.name.fl_str_mv Brazilian Journal of Pharmaceutical Sciences - Universidade de São Paulo (USP)
repository.mail.fl_str_mv bjps@usp.br||elizabeth.igne@gmail.com
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