Ginkgolide B Maintains Calcium Homeostasis in Hypoxic Hippocampal Neurons by Inhibiting Calcium Influx and Intracellular Calcium Release
Autor: | Wang Li, Ran Jihua, Quan Lei, Shuai Zhao, Wei Dong, Shi Qinghai, Xu Wenjuan, JianFeng Fu |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
ginkgolide B Ryanodine receptor 2 Calcium in biology lcsh:RC321-571 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine homeostasis medicine lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry Original Research Calcium metabolism Ryanodine receptor Chemistry hypoxia Hypoxia (medical) neuron Cell biology 030104 developmental biology medicine.anatomical_structure Cellular Neuroscience cytoplasmic calcium Neuron medicine.symptom 030217 neurology & neurosurgery Intracellular Homeostasis |
Zdroj: | Frontiers in Cellular Neuroscience, Vol 14 (2021) Frontiers in Cellular Neuroscience |
ISSN: | 1662-5102 |
Popis: | Ginkgolide B (GB), a terpene lactone and active ingredient of Ginkgo biloba, shows protective effects in neuronal cells subjected to hypoxia. We investigated whether GB might protect neurons from hypoxic injury through regulation of neuronal Ca2+ homeostasis. Primary hippocampal neurons subjected to chemical hypoxia (0.7 mM CoCl2) in vitro exhibited an increase in cytoplasmic Ca2+ (measured from the fluorescence of fluo-4), but this effect was significantly diminished by pre-treatment with 0.4 mM GB. Electrophysiological recordings from the brain slices of rats exposed to hypoxia in vivo revealed increases in spontaneous discharge frequency, action potential frequency and calcium current magnitude, and all these effects of hypoxia were suppressed by pre-treatment with 12 mg/kg GB. Western blot analysis demonstrated that hypoxia was associated with enhanced mRNA and protein expressions of Cav1.2 (a voltage-gated Ca2+ channel), STIM1 (a regulator of store-operated Ca2+ entry) and RyR2 (isoforms of Ryanodine Receptor which mediates sarcoplasmic reticulum Ca2+ release), and these actions of hypoxia were suppressed by GB. Taken together, our in vitro and in vivo data suggest that GB might protect neurons from hypoxia, in part, by regulating Ca2+ influx and intracellular Ca2+ release to maintain Ca2+ homeostasis. |
Databáze: | OpenAIRE |
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