Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

7-Piperazine ethyl chrysin inhibits proliferation of lung cancer cells via induction of apoptosis

Di Li¹, Lifei Li², Lingzhan Wang³, Jianguo Li¹, Bin Zhang^4-6

¹Department of Anatomy, The Medical College of Inner Mongolia University for the Nationalities; ²Respiratory Medicine, Affiliated Hospital of Inner Mongolia University for the Nationalities; ³Institute of Applied Anatomy; ⁴Medicinal Chemistry and Pharmacology Institute, Inner Mongolia University for Nationalities; ⁵Inner Mongolia Key Laboratory of Mongolian Medicine Pharmacology for Cardio-Cerebral Vascular System; ⁶Affiliated Hospital of Inner Mongolia University for Nationalities, Institute of Mongolia and Western Medicinal treatment, Inner Mongolia, 028000, China.

For correspondence:- Bin Zhang Email: BobbyyRobertskn@yahoo.com Tel:+864758314245

Accepted: 22 September 2018 Published: 31 October 2018

Citation: Li D, Li L, Wang L, Li J, Zhang B. 7-Piperazine ethyl chrysin inhibits proliferation of lung cancer cells via induction of apoptosis. Trop J Pharm Res 2018; 17(10):1919-1924 doi: 10.4314/tjpr.v17i10.4

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of 7-piperazine ethyl chrysin (PEC) on A-427 and A-549 lung cancer cell lines.

Methods: The cell lines were incubated with PEC at doses of 2, 4, 6, 8 and 10 µM for 24, 48 and 72 h, and their viabilities at each time interval were assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell apoptosis was evaluated with annexin V fluorescein isothiocyanate/propidium iodide staining, while the expression of ERK1/2 protein was determined using western blot. The involvement of ERK1/2 in the effect of PEC on viability and apoptosis was assessed by incubating the cells with PD98059 (an inhibitor of ERK1/2).

Results: Exposure to PEC at doses ≥ 4 µM significantly reduced the viability of A-427 and A-549 cell lines in time- and concentration-dependent manners at 48 h (p < 0.02). The viability of A-427 and A-549 cells was reduced to 21 and 18 %, respectively, on treatment with 8 µM PEC for 48 h. Moreover, PEC treatment induced apoptosis in A-427 (59.67 %) and A-549 (61.37 %) cells after 48 h. Western blot data revealed that PEC also significantly inhibited phosphorylation of ERK1/2 in both cancer cell lines (p < 0.05). Incubation of A-427 and A-549 cells with PD98059 for 48 h also reduced their viability and induced their apoptosis (p < 0.05).

Conclusion: These results indicate that PEC inhibits the viability of lung cancer cells via inhibition of ERK1/2 expression. Thus, PEC may be efective for the treatment of lung carcinoma but further studies are required to ascertain this.

Keywords: 7-Piperazine ethyl chrysin, Lung cancer cells, Apoptosis, Viability, inhibition