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Article: Apoptotic and cytotoxic effects on human glioblastoma cell lines induced by essential oil Lavandula Augustifolia

TitleApoptotic and cytotoxic effects on human glioblastoma cell lines induced by essential oil Lavandula Augustifolia
Authors
Keywordsapoptosis
cell viability
essential oil
glioblastoma
necrosis
Issue Date2020
Citation
Surgical Practice, 2020, v. 24, n. 1, p. 11-18 How to Cite?
AbstractAim: The challenge of treating glioblastoma has been the lack of curative treatment. This study aimed to identify an effective low dose of the essential oil from Lavandula angustifolia (EOla), within a short exposure time for inhibiting growth and inducing apoptosis in glioblastoma cells. Methods: Cell lines U-87MG and U-138MG were treated with diluted EOla (1:250 to 1:50) at 2, 4, 8 and 48 hours time points. The treated samples were compared with the negative control and DMSO vehicle control in MTT anti-proliferation tests and flow cytometry cell sorting experiments. A positive control (DNase I) was included in the TUNEL imaging assay. Results: Our data consistently showed that diluted EOla started inducing apoptosis at 1:250 dilution in both U-138MG and U-87MG samples. Significant differences in cell viability between DMSO and EOla samples were found in U-87MG, (P =.02) and U-138MG, (P =.003). Our flow cytometry results demonstrated that glioblastoma cells exposed to 1:100 diluted EOla for 4 hours had induced cell death in U-87MG with 94.9% ± 2.6 apoptosis and 1.7% ± 2.2 necrosis; and in U-138MG with 99% ± 3.3 apoptosis and 9.8% ± 3.1 necrosis. Conclusion: Unadulterated pure therapeutic grade EOla at the concentration of 1:100 dilution has been shown to induce predominantly apoptosis (>95%) with limited necrosis (1%-10%).
Persistent Identifierhttp://hdl.handle.net/10722/325471
ISSN
2023 Impact Factor: 0.3
2023 SCImago Journal Rankings: 0.152
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, Siu Yee-
dc.contributor.authorLi, Yi-
dc.contributor.authorPoon, Wai Sang-
dc.date.accessioned2023-02-27T07:33:34Z-
dc.date.available2023-02-27T07:33:34Z-
dc.date.issued2020-
dc.identifier.citationSurgical Practice, 2020, v. 24, n. 1, p. 11-18-
dc.identifier.issn1744-1625-
dc.identifier.urihttp://hdl.handle.net/10722/325471-
dc.description.abstractAim: The challenge of treating glioblastoma has been the lack of curative treatment. This study aimed to identify an effective low dose of the essential oil from Lavandula angustifolia (EOla), within a short exposure time for inhibiting growth and inducing apoptosis in glioblastoma cells. Methods: Cell lines U-87MG and U-138MG were treated with diluted EOla (1:250 to 1:50) at 2, 4, 8 and 48 hours time points. The treated samples were compared with the negative control and DMSO vehicle control in MTT anti-proliferation tests and flow cytometry cell sorting experiments. A positive control (DNase I) was included in the TUNEL imaging assay. Results: Our data consistently showed that diluted EOla started inducing apoptosis at 1:250 dilution in both U-138MG and U-87MG samples. Significant differences in cell viability between DMSO and EOla samples were found in U-87MG, (P =.02) and U-138MG, (P =.003). Our flow cytometry results demonstrated that glioblastoma cells exposed to 1:100 diluted EOla for 4 hours had induced cell death in U-87MG with 94.9% ± 2.6 apoptosis and 1.7% ± 2.2 necrosis; and in U-138MG with 99% ± 3.3 apoptosis and 9.8% ± 3.1 necrosis. Conclusion: Unadulterated pure therapeutic grade EOla at the concentration of 1:100 dilution has been shown to induce predominantly apoptosis (>95%) with limited necrosis (1%-10%).-
dc.languageeng-
dc.relation.ispartofSurgical Practice-
dc.subjectapoptosis-
dc.subjectcell viability-
dc.subjectessential oil-
dc.subjectglioblastoma-
dc.subjectnecrosis-
dc.titleApoptotic and cytotoxic effects on human glioblastoma cell lines induced by essential oil Lavandula Augustifolia-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/1744-1633.12406-
dc.identifier.scopuseid_2-s2.0-85081116894-
dc.identifier.volume24-
dc.identifier.issue1-
dc.identifier.spage11-
dc.identifier.epage18-
dc.identifier.eissn1744-1633-
dc.identifier.isiWOS:000514760700003-

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