Caffeine May Abrogate LPS-Induced Oxidative Stress and Neuroinflammation by Regulating Nrf2/TLR4 in Adult Mouse Brains
Badshah H, Ikram M, Ali W, Ahmad S, Hahm JR, Kim MO
Biomolecules · 86 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- Animals
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
Based on full-text disclosure statement.
Publication
- Published
- 2019-11-08 · Biomolecules · vol. 9 · issue 11 · p. 719
- Publisher
- Multidisciplinary Digital Publishing Institute
- Cited
- 103 citations · more than 96% of similar papers · 4.9× the field average
- Impact
- Top 10% most cited in its field
- References
- 41 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Neuroinflammation and Neurodegeneration Mechanisms · Genomics, phytochemicals, and oxidative stress · Tryptophan and brain disorders
- Keywords
- Oxidative stress, Caffeine, Lipopolysaccharide, TLR4, Endocrinology, Neuroinflammation, Chemistry, Internal medicine, Lipid peroxidation, Reactive oxygen species, Apoptosis, Pharmacology, Receptor, Biology, Medicine, Inflammation, Biochemistry
- MeSH
- brain, nerve tissue, animals, humans, mice, inflammation, reactive oxygen species, caffeine, jnk mitogen-activated protein kinases, lipopolysaccharides, nf-kappa b, membrane proteins, antioxidants, apoptosis, gene expression regulation, lipid peroxidation, oxidative stress, toll-like receptor 4, nf-e2-related factor 2, heme oxygenase-1
6 authors
From KR
- Haroon BadshahGyeongsang National University
- Muhammad Aimen IkramGyeongsang National University
- Waqar AliGyeongsang National University
- Sareer AhmadGyeongsang National University
- Jong Ryeal HahmGyeongsang National University Hospital
- Myeong Ok Kim · correspondingGyeongsang National University
Abstract
Herein, we assayed the antioxidant and anti-inflammatory potential of caffeine in a lipopolysaccharide (LPS)-injected mouse model of neurodegeneration and synaptic impairment. For this purpose, LPS was injected for two weeks on an alternate-day basis (250 µg/kg/i.p. for a total of seven doses), while caffeine was injected daily for four weeks (30 mg/kg/i.p/four weeks). According to our findings, there was a significant increase in the level of reactive oxygen species (ROS), as evaluated from the levels of lipid peroxidation (LPO) and ROS assays. Also, we evaluated the expression of nuclear factor erythroid-2-related factor 2 (Nrf2) and the enzyme hemeoxygenase 1 (HO-1) in the mouse groups and found reduced expression of Nrf2 and HO-1 in the LPS-treated mice brains, but they were markedly upregulated in the LPS + caffeine co-treated group. We also noted enhanced expression of toll-Like Receptor 4 (TLR4), phospho-nuclear factor kappa B (p-NF-kB), and phospho-c-Jun n-terminal kinase (p-JNK) in the LPS-treated mice brains, which was significantly reduced in the LPS + caffeine co-treated group. Moreover, we found enhanced expression of Bcl2-associated X, apoptosis regulator (Bax), and cleaved caspase-3, and reduced expression of B-cell lymphoma 2 (Bcl-2) in the LPS-treated group, which were markedly reversed in the LPS + caffeine co-treated group. Furthermore, we analyzed the expression of synaptic proteins in the treated groups and found a marked reduction in the expression of synaptic markers in the LPS-treated group; these were significantly upregulated in the LPS + caffeine co-treated group. In summary, we conclude that caffeine may inhibit LPS-induced oxidative stress, neuroinflammation, and synaptic dysfunction.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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