Ginkgolide Okay protects SH‑SY5Y cells towards oxygen‑glucose deprivation‑induced damage by inhibiting the p38 and JNK signaling pathways.
PMID:
Mol Med Rep. 2018 Sep ;18(3):3185-3192. Epub 2018 Jul 23. PMID: 30066915
Summary Title:
Ginkgolide Okay protects SH‑SY5Y cells towards oxygen‑glucose deprivation‑induced damage by inhibiting the p38 and JNK signaling pathways.
Summary:
The aim of the current research was to discover the protecting impact and purposeful mechanism of ginkgolide Okay (GK: C20H22O9) on cerebral ischemia. SH‑SY5Y cells had been uncovered to oxygen‑glucose deprivation (OGD) to simulate an ischemic mannequin in vitro. Cell viability, reactive oxygen species (ROS), nuclear staining with Hoechst 33258 and mitochondrial membrane potential had been detected following 4 h of publicity to OGD. Subsequently, the expression ranges of the apoptosis‑associated proteins, caspase‑9, caspase‑3, Bcl‑2, Bax, p53 and c‑Jun, as nicely because the mitogen‑activated protein kinases (MAPKs) signaling molecules had been detected by western blot evaluation. GK considerably elevated the cell viability and decreased the technology of ROS and the variety of apoptotic cells in a dose‑dependent method. Moreover, GK markedly decreased the protein expression ranges of p‑p38, p‑JNK, p‑p53, p‑c‑Jun and the expression ranges of Bcl‑2, Bax, cleaved caspase‑9 and caspase‑3. In conclusion, GK demonstrated a neuroprotective impact on the simulated cerebral ischemia in vitro, and this impact was mediated via the inhibition of the mitochondria‑mediated apoptosis pathway triggered by ROS‑evoked p38 and JNK activation.
