ArticleFrontiers in cellular neuroscience2018
Microglial Activation Is Modulated by Captopril:
Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Captopril restores microglial homeostasis and reverses ASD-like phenotype in a model of ASD induced by exposure in utero to anti-caspr2 IgG.Molecular psychiatry · 2026Article
- The Role of Rho-associated Kinase in the Cognitive Benefits of the ACE Inhibitory Peptide LAP for Hypertension.Current molecular medicine · 2026Article
- Biochemical, histopathological, and immunohistochemical study on the ameliorative effect of crocin against lipopolysaccharide‑induced hippocampal toxicity in male albino rats.BMC pharmacology & toxicology · 2025Article
- Association among blood pressure, antihypertensive drugs, and amyotrophic lateral sclerosis.Arquivos de neuro-psiquiatria · 2025Article
- Hypertension and hyperhomocysteinemia as modifiable risk factors for Alzheimer's disease and dementia: New evidence, potential therapeutic strategies, and biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Review
- Deciphering mechanisms of action of ACE inhibitors in neurodegeneration usingFrontiers in neuroscience · 2023Review
- Neuroinflammation as a mechanism linking hypertension with the increased risk of Alzheimer's disease.Neural regeneration research · 2022Review
- Captopril alleviates epilepsy and cognitive impairment by attenuation of C3-mediated inflammation and synaptic phagocytosis.Journal of neuroinflammation · 2022Article
- Angiotensin II related glial cell activation and necroptosis of retinal ganglion cells after systemic hypotension in glaucoma.Cell death & disease · 2022Article
- Captopril exhibits protective effects through anti-inflammatory and anti-apoptotic pathways against hydrogen peroxide-induced oxidative stress in C6 glioma cells.Metabolic brain disease · 2022Article
- Captopril is more effective than Perindopril against aluminium chloride induced amyloidogenesis and AD like pathology.Heliyon · 2022Article
- Vascular smooth muscle cell dysfunction in neurodegeneration.Frontiers in neuroscience · 2022Review
- Pharmaceutical Potential of Casein-Derived Tripeptide Met-Lys-Pro: Improvement in Cognitive Impairments and Suppression of Inflammation in APP/PS1 Mice.Journal of Alzheimer's disease : JAD · 2022Article
- Captopril Combined with Furosemide or Hydrochlorothiazide Affects Macrophage Functions in Mouse Contact Hypersensitivity Response.International journal of molecular sciences · 2021Article
- Anti-Inflammatory Activities of Captopril and Diuretics on Macrophage Activity in Mouse Humoral Immune Response.International journal of molecular sciences · 2021Article
- Vascular smooth muscle cell dysfunction contribute to neuroinflammation and Tau hyperphosphorylation in Alzheimer disease.iScience · 2021Article
- Brain Renin-Angiotensin System as Novel and Potential Therapeutic Target for Alzheimer's Disease.International journal of molecular sciences · 2021Review
- The Neurovascular Unit Dysfunction in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Recent Advances in the Endogenous Brain Renin-Angiotensin System and Drugs Acting on It.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2021Review
- Maternal Treatment With Captopril Persistently Alters Gut-Brain Communication and Attenuates Hypertension of Male Offspring.Hypertension (Dallas, Tex. : 1979) · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The renin-angiotensin system (RAS) is an important peripheral system involved in homeostasis modulation, with angiotensin II (Ang II) serving as the main effector hormone. The main enzyme involved in Ang II formation is angiotensin-converting enzyme (ACE). ACE inhibitors (ACEIs) such as captopril (Cap) are predominantly used for the management of hypertension. All of the components of the RAS have also been identified in brain. Centrally located hormones such as Ang II can induce glial inflammation. Moreover, in Alzheimer's disease (AD) models, where glial inflammation occurs and is thought to contribute to the propagation of the disease, increased levels of Ang II and ACE have been detected. Interestingly, ACE overexpression in monocytes, migrating to the brain was shown to prevent AD cognitive decline. However, the specific effects of captopril on glial inflammation and AD remain obscure. In the present study, we investigated the effect of captopril, given at a wide concentration range, on inflammatory mediators released by lipopolysaccharide (LPS)-treated glia. In the current study, both primary glial cells and the BV2 microglial cell line were used. Captopril decreased LPS-induced nitric oxide (NO) release from primary mixed glial cells as well as regulating inducible NO synthase (iNOS) expression, NO, tumor necrosis factor-α (TNF-α) and induced interleukin-10 (IL-10) production by BV2 microglia. We further obtained data regarding intranasal effects of captopril on cortical amyloid β (Aβ) and CD11b expression in 5XFAD cortex over three different time periods. Interestingly, we noted decreases in Aβ burden in captopril-treated mice over time which was paralleled by increased microglial activation. These results thus shed light on the neuroprotective role of captopril in AD which might be related to modulation of microglial activation.
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Registered trials
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