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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.

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