Chenopodium Botrys as a Source of Sesquiterpenes to Induce Apoptosis and G1 Cell Cycle Arrest in Cervical Cancer Cells

Document Type: Research article

Authors

1 Traditional and Complementary Medicine Research Center, Sabzevar University of Medical Sciences, Sabzevar, Iran.

2 Cellular and Molecular Research center, Sabzevar University of Medical Sciences, Sabzevar, Iran. Immunology Research Center, Bu-Ali Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran. dDepartment of Chemistry, Sabzevar Branch, Islamic Azad University, Sabzevar, Iran.

3 Department of Chemistry, Faculty of Science, Islamic Azad University of Sabzevar, Sabzevar, Iran.

Abstract

Conducting cell apoptosis pathways is a novel strategy in cancer treatment. This study aimed to explain that C. botrys essential oil could induce apoptosis and arrest the cell cycle in HeLa cells. Cytotoxic and apoptogenic effects of the essential oil of Jerusalem-oak (Chenopodium botrys L.), which was obtained from the aerial parts of the plant, were evaluated in HeLa cells. Cell viability was assessed by MTT and LDH assays, and the mechanism of cell apoptosis was investigated using flow cytometry. Expression of the apoptosis-related genes was assessed using real-time polymerase chain reaction (PCR). GC-MS analysis of the herbal essential oil revealed 37 components. The major components were α-Eudesmol (16.81%), Elemol acetate (13.2%), Elemol (9.0%), and α-Chenopodiol-6-acetate (7.9%). The essential oil inhibited the growth of HeLa cells and increased the expression of p21 and p53. In addition, essential oil treatment increased the sub-G1 DNA content and induced apoptosis due to the increased Bax/Bcl-2 ratio and up-regulation of caspase-3 gene expression. According to the results, C. botrys essential oil exhibited anticancer effects through intrinsic apoptosis pathways and arresting cell proliferation.

Graphical Abstract

Chenopodium Botrys as a Source of Sesquiterpenes to Induce Apoptosis and G1 Cell Cycle Arrest in Cervical Cancer Cells

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