Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Anthocyanin attenuates oxygen-glucose deprivation/reperfusion-induced apoptosis of PC12 cells via inactivation of ASK1/JNK/p38 signaling pathway

Hong Zhu¹, Dan Ren¹, Lan Xiao¹ , Ting Zhang¹, Ruomeng Li¹, Bin Guan¹, Jing Zhang²

¹Department of Traditional Chinese Medicine, Central South University Third Xiangya Hospital, Hunan 410013, China; ²Department of Thoracic Internal Medicine, Hunan Cancer Hospital, Huanan 410013, China.

For correspondence:- Lan Xiao Email: LanXiaoLX1103@163.com Tel:+8673188618209

Accepted: 21 September 2019 Published: 31 October 2019

Citation: Zhu H, Ren D, Xiao L, Zhang T, Li R, Guan B, et al. Anthocyanin attenuates oxygen-glucose deprivation/reperfusion-induced apoptosis of PC12 cells via inactivation of ASK1/JNK/p38 signaling pathway. Trop J Pharm Res 2019; 18(10):2037-2043 doi: 10.4314/tjpr.v18i10.6

© 2019 The authors.
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Abstract

Purpose: To investigate whether the cytoprotective effect of anthocyanin (Anc) on oxygen-glucose deprivation/reperfusion (OGD/R)-induced cell injury is related to apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK)/p38 signaling pathway.

Methods: PC12 cells were pre-treated with various concentrations of Anc (10, 50, and 100 μg/mL) in OGD/R-induced cell injury model. The 3-(4, 5)-dimethylthiahiazo (-z-y1)-3, 5-di-phenytetrazoliumromide (MTT) assay was used to assess cell viability. Cell apoptosis was measured by lactic acid dehydrogenase (LDH) release assay and flow cytometry. Western blot was employed to determine the protein expressions of BCL-2, BAX, caspase-3, p-ASK1 (Thr845), p-JNK, and p-p38.

Results: The results indicate that Anc increased the viability of PC12 cells after OGD/R exposure (p < 0.05), and also efficiently rescued OGD/R-induced apoptosis (p < 0.05). Mechanistic studies showed that these protective roles of Anc are related to the inhibition of ASK1/JNK/p38 signaling pathway.

Conclusion: The results indicate Anc protects against OGD/R-induced cell injury by enhancing cell viability and inhibiting cell apoptosis. The underlying mechanism of action is partly via inactivation of ASK1/JNK/p38 signaling pathway. Thus, Anc has promise as a potential natural agent to prevent and treat cerebral ischemia-reperfusion injury.

Keywords: Cerebral ischemia-reperfusion injury, OGD/R, Anthocyanin, ASK1/JNK/p38 signaling pathways, Cell apoptosis