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Selenium-containing protein from selenium-enriched Spirulina platensis antagonizes oxygen glucose deprivation-induced neurotoxicity by inhibiting ROS-mediated oxidative damage through regulating MPTP opening.

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机构: [1]Department of Neurology, Guangzhou University of Chinese Medicine, Guangzhou, China [2]Department of Neurology, Linyi People’s Hospital, Linyi, China [3]Department of Internal Medicine, Taian Traffic Hospital, Taian, China [4]CAS Key Laboratory of Tropical Marine Bio-resources and Ecology (LMB-CAS), Guangdong Key Laboratory of Marine Materia Medica (LMMM-GD), South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, China [5]Department of Rehabilitation, Taian City Central Hospital, Taian, China Shandong [6]Department of Neurosurgery, Taian City Central Hospital, Taian, China
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关键词: Ischaemic brain injury apoptosis neurons mitochondrial dysfunction

摘要:
Selenium-containing protein from selenium-enriched Spirulina platensis (Se-SP) (syn. Arthrospira platensis [Microcoleaceae]) showed novel antioxidant activity. However, the protective effect of Se-SP against oxygen glucose deprivation (OGD)-induced neural apoptosis has not been reported yet.To verify whether Se-SP can inhibit OGD-induced neural apoptosis and explore the underlying mechanism.Primary hippocampal neurons were separated from Sprague-Dawley (SD) rats. 95% N2 + 5% CO2 were employed to establish OGD model. Neurons were treated with 5 and 10 µg/mL Se-SP under OGD condition for 6 h. Neurons without treatment were the control group. Neural viability and apoptosis were detected by MTT, immunofluorescence and western blotting methods.Se-SP significantly improved neuronal viability (from 57.2% to 94.5%) and inhibited apoptosis in OGD-treated primary neurons (from 45.6% to 6.3%), followed by improved neuronal morphology and caspases activation. Se-SP co-treatment also effectively suppressed OGD-induced DNA damage by inhibiting ROS accumulation in neurons (from 225.6% to 106.3%). Additionally, mitochondrial dysfunction was also markedly improved by Se-SP co-treatment via balancing Bcl-2 family expression. Moreover, inhibition of mitochondrial permeability transition pore (MPTP) by CsA (an MPTP inhibitor) dramatically attenuated OGD-induced ROS generation (from 100% to 56.2%), oxidative damage, mitochondrial membrane potential (MPP) loss (from 7.5% to 44.3%), and eventually reversed the neuronal toxicity and apoptosis (from 57.4% to 79.6%).Se-SP showed enhanced potential to inhibit OGD-induced neurotoxicity and apoptosis by inhibiting ROS-mediated oxidative damage through regulating MPTP opening, indicating that selenium-containing protein showed broad application in the chemoprevention and chemotherapy against human ischaemic brain injury.

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出版当年[2020]版:
大类 | 3 区 医学
小类 | 3 区 医学实验技术 3 区 药学 3 区 植物科学
最新[2025]版:
大类 | 3 区 医学
小类 | 2 区 医学实验技术 2 区 药学 2 区 植物科学
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第一作者机构: [1]Department of Neurology, Guangzhou University of Chinese Medicine, Guangzhou, China [2]Department of Neurology, Linyi People’s Hospital, Linyi, China
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通讯机构: [2]Department of Neurology, Linyi People’s Hospital, Linyi, China [5]Department of Rehabilitation, Taian City Central Hospital, Taian, China Shandong [6]Department of Neurosurgery, Taian City Central Hospital, Taian, China [*1]Department of Neurosurgery, Taian City Central Hospital, Longtan Road, Taian 271000, China [*2]Department of Neurology, Linyi People’s Hospital, Jiefang Road East Section No.27, Linyi 276000, China [*3]Department of Rehabilitation, Taian City Central Hospital, Longtan Road, Taian 271000, China
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