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