ArticleMolecular medicine reports2018
Ginkgolide K protects SH‑SY5Y cells against oxygen‑glucose deprivation‑induced injury by inhibiting the p38 and JNK signaling pathways.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Natural products regulate mitochondrial function in cognitive dysfunction-A scoping review.Frontiers in pharmacology · 2023Article
- Traditional Chinese medicine in treating ischemic stroke by modulating mitochondria: A comprehensive overview of experimental studies.Frontiers in pharmacology · 2023Review
- Protective Effect ofNutrients · 2022Article
- Effect of ginkgolide K on calcium channel activity in Alzheimer's disease.Experimental and therapeutic medicine · 2022Article
- Therapeutic targets by traditional Chinese medicine for ischemia-reperfusion injury induced apoptosis on cardiovascular and cerebrovascular diseases.Frontiers in pharmacology · 2022Review
- Antioxidant effects of ginkgolides and bilobalide against cerebral ischemia injury by activating the Akt/Nrf2 pathway in vitro and in vivo.Cell stress & chaperones · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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