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Vitamin D Activates Nrf2 to Prevent Nerve Injury and Reduce Brain Damage in Acute Cerebral Infarction
Hong-Min Zhao1, Li-Qin Mu1, Jing Wang1
1Department of General Practice, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, China.
Current Medical Science
|May 7, 2025
Summary
Cholecalciferol cholesterol emulsion (CCE), a vitamin D precursor, demonstrated significant neuroprotective effects in a murine model of acute cerebral infarction (ACI). These benefits were mediated by the Nrf2/HO-1 pathway, reducing inflammation and apoptosis.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Acute cerebral infarction (ACI) poses a significant health challenge, necessitating novel therapeutic strategies.
- Vitamin D (VD) is increasingly recognized for its potential roles beyond bone health, including neuroprotection.
- The Nrf2 signaling pathway is a critical regulator of cellular defense against oxidative stress and inflammation.
Purpose of the Study:
- To investigate the neuroprotective effects of cholecalciferol cholesterol emulsion (CCE), a vitamin D precursor, in a murine model of acute cerebral infarction (ACI).
- To elucidate the role of the Nrf2 signaling pathway in mediating the neuroprotective effects of CCE.
- To assess the impact of CCE on neurological function, brain edema, infarct size, and molecular markers of inflammation and apoptosis.
Main Methods:
- Forty C57BL/6J mice were divided into five groups: control, control+CCE, ACI, ACI+CCE, and ACI+CCE+ML385 (Nrf2 inhibitor).
- ACI was induced via middle cerebral artery occlusion (MCAO).
- CCE was administered for three weeks prior to MCAO, and ML385 was used to inhibit Nrf2. Neurological function, brain edema, infarct size, and inflammatory/apoptotic markers were assessed.
Main Results:
- CCE significantly reduced neurological deficits, brain edema, and infarct size in ACI mice (P < 0.01).
- CCE improved short-term memory retention and attenuated inflammatory markers (IL-6, MIF, Lp-PLA2) while increasing IL-10.
- CCE increased Nrf2 and HO-1 expression, reduced apoptosis (Bax/Bcl-2 ratio), and these effects were abolished by ML385.
Conclusions:
- Vitamin D (VD), through VD receptor-mediated activation of the Nrf2/HO-1 pathway, confers neuroprotection in ACI.
- CCE effectively reduces inflammation, apoptosis, and neurological damage following ischemic stroke.
- These findings highlight the therapeutic potential of VD in ischemic stroke treatment, emphasizing the crucial role of Nrf2.
Keywords:
Acute cerebral infarctionApoptosisCholecalciferol cholesterol emulsionNeuroprotectionNrf2 signaling pathwayVitamin DMore Related Videos
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