Curcumin Inhibits Aβ-Induced Microglial Inflammatory Responses In Vitro: Involvement of ERK1/2 and P38 Signaling Pathways
Abstract
Amyloid β (Aβ) plays an important role in Alzheimer's disease (AD) by inducing microglia activation. Once activated, microglial cells promote the release of reactive species and cytokines that are known to enhance immune responses in AD brain. Thus, negative regulators of microglia activation are considered as potential therapeutic candidates for AD. Curcumin, the major yellow pigment in turmeric (Curcuma longa), is proposed for its anti-inflammatory properties. Several studies have indicated the suppressive effects of curcumin on LPS-induced microglia activation and MAPK activities. However, the effects of curcumin on Aβ-treated microglia and the possible mechanisms are still not fully understood. In the present study, we found that curcumin improved microglial viability against Aβ42 in a time- and dose-dependent manner and remarkably suppressed Aβ42-induced CD68 expression. Moreover, curcumin concentration-dependently abolished Aβ42-induced interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) production in mRNA and protein levels in microglia. Besides, curcumin exerted an inhibitory effect on phosphorylation of ERK1/2 and p38 in Aβ42-activated microglia. Further experiments indicated that blockage of ERK1/2 and p38 pathways reduced inflammatory cytokines production from microglia. These results show that curcumin suppresses ERK1/2 and p38 signaling, thus, attenuating inflammatory responses of brain microglia.
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Curcumin decreases IL-1β, IL-6 and TNF-α expression in Aβ-activated microglia by inhibiting Erk1/2 and p38 MAPK pathways.
“curcumin has been shown to decrease in a concentration-dependent manner the expression of IL-1β, IL-6 and TNF-α in the Aβ-activated microglia by inhibiting Erk1/2 and p38 MAPK pathways (Shi et al., 2015)”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Shi et al., 2015
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- Authors
- Shi, X., Zheng, Z., Li, J., Xiao, Z., Qi, W., Zhang, A., Wu, Q., & Fang, Y.
- Affiliations
- Sun Yat-sen University (CN)
- Corresponding author
- Wu, Qi
- Fang, Yannan
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2015-05
- Volume
- 594
- Pages
- 105-110
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2000667575
- Cited by
- 108
- References
- 24
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 7 · 2023: 11 · 2022: 14 · 2021: 9 · 2020: 10 · 2019: 7 · 2018: 12 · 2017: 12 · 2016: 9 · 2015: 3
- FWCI
- 4.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China
- Sun Yat-sen University
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Curcumin's Biomedical Applications
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- curcumin, amyloid-beta, amyloid-beta 42, microglial activation, neuroinflammation, Alzheimer's disease, ERK signaling, p38 MAPK, inflammatory cytokines, CD68, anti-inflammatory activity
- MeSH terms
- Animals, Animals, Newborn, Anti-Inflammatory Agents, Cells, Cultured, Curcumin, Mice, Inbred BALB C, Peptide Fragments, Phosphorylation, RNA, Messenger, Tumor Necrosis Factor-alpha, Interleukin-6, Amyloid beta-Peptides, Microglia, Mitogen-Activated Protein Kinase 1, MAP Kinase Signaling System, p38 Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase 3, Interleukin-1beta
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