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Menaquinone-7 protects astrocytes by regulating mitochondrial function and inflammatory response under hypoxic
1Department of Histology and Embryology, Medical College, Nantong University, Nantong, China. wxdzw@ntu.edu.cn.
European Review for Medical and Pharmacological Sciences
|October 22, 2020
Summary
Menaquinone-7 (MK-7) protects astrocytes from hypoxic brain injury by improving cell viability and reducing inflammation. This vitamin K2 (VK2) derivative may also involve growth arrest-specific 6 (Gas6) in its protective mechanisms.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Astrocytes are crucial in brain injury, particularly during hypoxia.
- Hypoxia significantly impairs astrocyte function and survival.
- Understanding protective mechanisms against hypoxic astrocyte damage is vital.
Purpose of the Study:
- To investigate the protective effects of menaquinone-7 (MK-7), a vitamin K2 (VK2) subtype, on astrocytes under hypoxic conditions.
- To elucidate the potential mechanisms underlying MK-7's effects, including its impact on reactive oxygen species (ROS), ATP production, and inflammatory markers.
- To explore the role of growth arrest-specific 6 (Gas6) in MK-7's neuroprotective actions.
Main Methods:
- Primary astrocyte cultures from Sprague Dawley rats were subjected to a hypoxia model.
- Cell Counting Kit-8 (CCK-8) and BrdU assays assessed cell viability and proliferation.
- Reactive oxygen species (ROS) levels were measured using DCFDA and DHE assays.
- ATP production was quantified, and levels of cytokines (IL-6, TNF-α) and chemokines (CCL2, CXCL10) were determined.
- Growth arrest-specific 6 (Gas6) expression and function were analyzed, including siRNA knockdown experiments.
Main Results:
- Hypoxia significantly reduced astrocyte viability and proliferation, which was reversed by MK-7 pretreatment.
- MK-7 inhibited hypoxia-induced ROS production and enhanced ATP generation in astrocytes.
- MK-7 pretreatment decreased the expression of IL-6, TNF-α, CCL2, and CXCL10 while increasing Gas6 levels.
- Gas6 inhibition partially reversed the beneficial effects of MK-7 on ROS, IL-6, viability, and ATP production.
Conclusions:
- MK-7 demonstrates significant neuroprotective effects against hypoxia-induced astrocyte damage.
- These protective effects are likely mediated by the inhibition of mitochondrial dysfunction and pro-inflammatory cytokine expression.
- Growth arrest-specific 6 (Gas6) appears to play a role in the mechanisms of MK-7's protective actions in hypoxic astrocytes.
