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Updated: Feb 24, 2026
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Modafinil attenuates inflammation via inhibiting Akt/NF-κB pathway in apoE-deficient mouse model of atherosclerosis
Jinxia Han1, Dongwei Chen2, Dayi Liu3
1Department of Cardiology, Daqing Oil Field General Hospital, NO. 9 Saertu District, Daqing, 163000, Heilongjiang, China. hanjinxia79@163.com.
Abstract:
Modafinil, an FDA approved wakefulness drug prescribed to narcolepsy patients, has recently been shown to have anti-inflammatory effects and provides protection against neuroinflammation. It is unknown if modafinil can also protect against atherosclerosis, pathogenesis of which implicates inflammation. Using an apoE-deficient mouse model, we tried to elucidate the effects of modafinil treatment on the development of atherosclerosis. We tested serum levels of cytokines. We isolated mouse bone marrow-derived macrophages (BMDMs), detected effect of modafinil on the viability and proliferation of BMDMs, and on oxidized low-density lipoprotein-induced IL-6 and TNF-α, and supernatant level of IFN-γ as well as NF-κB activity in BMDMs. Modafinil inhibited the development of atherosclerosis in apoE-/- mice. Modafinil suppressed the secretion of pro-inflammatory cytokines IL-6, TNF and IFN-γ, and promoted secretion of anti-inflammatory cytokines IL-4 and IL-10. Modafinil inhibited viability and proliferation of macrophages by negatively regulating levels of pro-inflammatory cytokines, p-Akt, p-IKBα and NF-κB activity in macrophages. Modafinil mitigates inflammation in apoE-/- atherosclerosis mice via inhibiting NF-κB activity in macrophages, and could potentially serve as a therapeutic agent for atherosclerosis.
Insights
Modafinil, a wakefulness drug, was found to inhibit atherosclerosis development in mice. This study shows modafinil mitigates inflammation by targeting macrophage activity, suggesting potential therapeutic use for atherosclerosis.
Area of Science:
- Pharmacology
- Immunology
- Cardiovascular Research
Background:
- Modafinil, approved for narcolepsy, exhibits anti-inflammatory and neuroprotective properties.
- Atherosclerosis pathogenesis involves inflammation, but modafinil's role is unexplored.
- Investigating modafinil's potential in mitigating atherosclerosis is crucial.
Purpose of the Study:
- To determine if modafinil treatment protects against atherosclerosis development.
- To elucidate the anti-inflammatory mechanisms of modafinil in an atherosclerosis model.
Main Methods:
- Utilized apolipoprotein E-deficient (apoE-/-) mice to model atherosclerosis.
- Assessed serum cytokine levels and macrophage (BMDM) responses to modafinil.
- Analyzed modafinil's effects on macrophage viability, proliferation, cytokine secretion, and NF-κB pathway activation.
Main Results:
- Modafinil significantly inhibited atherosclerosis progression in apoE-/- mice.
- Modafinil suppressed pro-inflammatory cytokines (IL-6, TNF-α, IFN-γ) and promoted anti-inflammatory cytokines (IL-4, IL-10).
- Modafinil reduced macrophage viability and proliferation by downregulating NF-κB activity, p-Akt, and p-IKBα.
Conclusions:
- Modafinil mitigates inflammation in atherosclerosis by inhibiting NF-κB activity in macrophages.
- Modafinil demonstrates potential as a therapeutic agent for atherosclerosis.
- Further research into modafinil's cardiovascular benefits is warranted.
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