Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Protective effect of liquiritin on corticosterone-induced neurotoxicity in PC12 cells

Jing Wu¹ , Fei Xiang Huang², Jing Wang³, Chang Cheng Shi⁴, Guo Ying Fang¹

¹Department of Pharmacy; ²Department of Traditional Chinese Medicine; ³Department of Obstetrics, Hangzhou Obstetrics & Gynecology Hospital, Hangzhou, Zhejiang 310008; ⁴Department of Pharmacy, Hangzhou First People's Hospital, Hangzhou, Zhejiang 310006, PR China.

For correspondence:- Jing Wu Email: wujing1_work@126.com Tel:+8657156005734

Accepted: 23 September 2018 Published: 31 October 2018

Citation: Wu J, Huang FX, Wang J, Shi CC, Fang GY. Protective effect of liquiritin on corticosterone-induced neurotoxicity in PC12 cells. Trop J Pharm Res 2018; 17(10):2013-2017 doi: 10.4314/tjpr.v17i10.17

© 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 determine the protective effects of liquiritin on corticosterone-induced neurotoxicity in rat pheochromocytoma (PC12) cells.

Methods: Neurotoxicity in PC12 cells was induced by different concentrations of corticosterone. Proliferation of PC12 cells was evaluated using CCK8 assay kits, while apoptosis was determined by flow cytometry.

Results: The results indicate that corticosterone inhibited the proliferation of PC12 cells time- and dose-dependently. The inhibitory effect (0.2 mM) was ameliorated by liquiritin. Furthermore, the cell apoptosis rate and protein level of caspase 3 in PC12 cells induced by corticosterone were ameliorated by liquiritin (1 and 2 mg/mL) treatment. Moreover, the protective effect of liquiritin (2 mg/mL) on corticosterone induced neurotoxicity in PC12 cells was weakened by K252a (the specific TrkB inhibitor) treatment. In addition, the protein level of brain-derived neurotrophic factor (BDNF) and (tyrosine-kinase receptor) TrkB showed a reverse trend to caspase 3.

Conclusion: Liquiritin shows protective effects against neurotoxicity induced by corticosterone in PC12 cells, and these effects are exerted via up-regulating BDNF/TrkB signaling.

Keywords: Liquiritin, Antidepressant, Corticosterone, Neuroprotection, PC12 cells, BDNF/TrkB signaling