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Article Open Access

Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways

  • Authors:
    • Qiu Liu
    • Xueke Li
    • Liang Li
    • Zhiliang Xu
    • Jun Zhou
    • Wei Xiao
  • View Affiliations / Copyright

    Affiliations: Jiangsu Kanion Pharmaceutical Co., Ltd., Jiangsu, Lianyungang 222001, P.R. China, State Key Laboratory of New‑Tech for Chinese Medicine Pharmaceutical Process, Jiangsu, Lianyungang 222001, P.R. China
    Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].
  • Pages: 3185-3192
    |
    Published online on: July 23, 2018
       https://doi.org/10.3892/mmr.2018.9305
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Abstract

The purpose of the present study was to explore the protective effect and functional mechanism of ginkgolide K (GK: C20H22O9) on cerebral ischemia. SH‑SY5Y cells were exposed to oxygen‑glucose deprivation (OGD) to simulate an ischemic model in vitro. Cell viability, reactive oxygen species (ROS), nuclear staining with Hoechst 33258 and mitochondrial membrane potential were detected following 4 h of exposure to OGD. Subsequently, the expression levels of the apoptosis‑related proteins, caspase‑9, caspase‑3, Bcl‑2, Bax, p53 and c‑Jun, as well as the mitogen‑activated protein kinases (MAPKs) signaling molecules were detected by western blot analysis. GK significantly elevated the cell viability and decreased the generation of ROS and the number of apoptotic cells in a dose‑dependent manner. Furthermore, GK markedly decreased the protein expression levels of p‑p38, p‑JNK, p‑p53, p‑c‑Jun and the expression levels of Bcl‑2, Bax, cleaved caspase‑9 and caspase‑3. In conclusion, GK demonstrated a neuroprotective effect on the simulated cerebral ischemia in vitro, and this effect was mediated through the inhibition of the mitochondria‑mediated apoptosis pathway triggered by ROS‑evoked p38 and JNK activation.
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Copy and paste a formatted citation
Spandidos Publications style
Liu Q, Li X, Li L, Xu Z, Zhou J and Xiao W: Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways. Mol Med Rep 18: 3185-3192, 2018.
APA
Liu, Q., Li, X., Li, L., Xu, Z., Zhou, J., & Xiao, W. (2018). Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways. Molecular Medicine Reports, 18, 3185-3192. https://doi.org/10.3892/mmr.2018.9305
MLA
Liu, Q., Li, X., Li, L., Xu, Z., Zhou, J., Xiao, W."Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways". Molecular Medicine Reports 18.3 (2018): 3185-3192.
Chicago
Liu, Q., Li, X., Li, L., Xu, Z., Zhou, J., Xiao, W."Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways". Molecular Medicine Reports 18, no. 3 (2018): 3185-3192. https://doi.org/10.3892/mmr.2018.9305
Copy and paste a formatted citation
x
Spandidos Publications style
Liu Q, Li X, Li L, Xu Z, Zhou J and Xiao W: Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways. Mol Med Rep 18: 3185-3192, 2018.
APA
Liu, Q., Li, X., Li, L., Xu, Z., Zhou, J., & Xiao, W. (2018). Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways. Molecular Medicine Reports, 18, 3185-3192. https://doi.org/10.3892/mmr.2018.9305
MLA
Liu, Q., Li, X., Li, L., Xu, Z., Zhou, J., Xiao, W."Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways". Molecular Medicine Reports 18.3 (2018): 3185-3192.
Chicago
Liu, Q., Li, X., Li, L., Xu, Z., Zhou, J., Xiao, W."Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways". Molecular Medicine Reports 18, no. 3 (2018): 3185-3192. https://doi.org/10.3892/mmr.2018.9305
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