Mangiferin decreases inflammation and oxidative damage in rat brain after stress
Abstract
Purpose Stress exposure elicits neuroinflammation and oxidative damage in brain, and stress-related neurological and neuropsychiatric diseases have been associated with cell damage and death. Mangiferin (MAG) is a polyphenolic compound abundant in the stem bark of Mangifera indica L. with antioxidant and anti-inflammatory properties in different experimental settings. In this study, the capacity of MAG to prevent neuroinflammation and brain oxidative damage induced by stress exposure was investigated. Methods Young-adult male Wistar rats immobilized during 6 h were administered by oral gavage with increasing doses of MAG (15, 30, and 60 mg/Kg), respectively, 7 days before stress. Results Prior treatment with MAG prevented all of the following stress-induced effects: (1) increase in glucocorticoids (GCs) and interleukin-1β (IL-1β) plasma levels, (2) loss of redox balance and reduction in catalase brain levels, (3) increase in pro-inflammatory mediators, such as tumor necrosis factor alpha TNF-α and its receptor TNF-R1, nuclear factor-kappa B (NF-κB) and synthesis enzymes, such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), (4) increase in lipid peroxidation. Conclusions These multifaceted protective effects suggest that MAG administration could be a new therapeutic strategy in neurological/neuropsychiatric pathologies in which hypothalamic/pituitary/adrenal (HPA) stress axis dysregulation, neuroinflammation, and oxidative damage take place in their pat…
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Pretreatment with mangiferin inhibits an increase in levels of glucocorticoids, IL-1beta, TNF-alpha, TNF receptor 1, NF-κB, iNOS and COX-2.
“Pretreatment with mangiferin inhibits an increase in the levels of glucocorticoids (GCs), IL-1β, TNF-α, TNF receptor 1, NF-κB, inducible nitric oxide synthase (iNOS) and COX-2 (73).”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [73]
Mangiferin administration (15, 30 and 60 mg/kg; oral gavage) prevents HPA stress axis dysregulation, neuroinflammation and oxidative damage.
“It was demonstrated that mangiferin administration (15, 30 and 60 mg/kg; oral gavage) prevents hypothalamic/pituitary/adrenal (HPA) stress axis dysregulation, neuroinflammation and oxidative damage.”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [73]
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- Authors
- Márquez, L., García-Bueno, B., Madrigal, J. L. M., & Leza, J. C.
- Affiliations
- Universidad Complutense de Madrid (ES)
- Corresponding author
- Leza, Juan C.
- Venue
- European Journal of Nutrition
- Published
- 2011-10-07
- Volume
- 51
- Issue
- 6
- Pages
- 729-739
- ISSN
- 1436-6207 (ISSN-L)
- 1436-6215
- OpenAlex
- W2047057122
- Cited by
- 111
- References
- 8
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 9 · 2023: 9 · 2022: 4 · 2021: 7 · 2020: 6 · 2019: 7 · 2018: 7 · 2017: 12 · 2016: 19 · 2015: 4 · 2014: 7 · 2013: 8 · 2012: 4
- FWCI
- 16.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- European Journal of Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Instituto de Salud Carlos III
- Topics
- Health Sciences › Medicine › Complementary and alternative medicine › Mangiferin and Mango Extracts
- Health Sciences › Nursing › Nutrition and Dietetics › Magnesium in Health and Disease
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- mangiferin, neuroinflammation, oxidative stress, brain, psychological stress, restraint stress, glucocorticoids, IL-1β, TNF-α, NF-κB, inducible nitric oxide synthase, cyclooxygenase-2, lipid peroxidation, catalase, hypothalamic-pituitary-adrenal axis, neuroprotection, polyphenols, mango
- MeSH terms
- Animals, Anti-Inflammatory Agents, Non-Steroidal, Antioxidants, Brain, Corticosterone, Dose-Response Relationship, Drug, Male, Nerve Tissue Proteins, Neurons, Random Allocation, Stress, Psychological, Lipid Peroxidation, Rats, Wistar, Oxidative Stress, Neuroprotective Agents, Inflammation Mediators, Ethnopharmacology, Xanthones, Receptors, Tumor Necrosis Factor, Type I, Rats, Cyclooxygenase 2, Nitric Oxide Synthase Type II
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