Abstract
Obesity is closely associated with neuroinflammation in the hypothalamus, which is characterized by over-activated microglia and excessive production of pro-inflammatory cytokines. The present study was aimed at elucidating the effects of (-)-epigallocatechin gallate (EGCG) on palmitic acid-stimulated BV-2 microglia and high-fat-diet-induced obese mice. The results indicated the suppressive effect of EGCG on lipid accumulation, pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) release, and microglial activation in both cellular and high-fat-diet rodent models. These results were associated with lower phosphorylated levels of the janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) signaling pathway. In conclusion, EGCG can attenuate high-fat-induced hypothalamic inflammation via inhibiting the JAK2/STAT3 signaling pathways in microglia.
Keywords:
hypothalamus; inflammation; obesity; saturated fatty acids; tea polyphenols.
MeSH terms
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Animals
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Anti-Obesity Agents / pharmacology*
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Anti-Obesity Agents / therapeutic use
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Catechin / analogs & derivatives*
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Catechin / pharmacology
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Catechin / therapeutic use
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Cell Line
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Diet, High-Fat / adverse effects
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Disease Models, Animal
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Hypothalamus / drug effects
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Hypothalamus / immunology
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Hypothalamus / metabolism
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Inflammation / metabolism
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Interleukin-1beta / metabolism
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Interleukin-6 / metabolism
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Janus Kinase 2 / metabolism
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Lipid Metabolism / drug effects
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Mice
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Mice, Inbred C57BL
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Mice, Obese
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Microglia / drug effects*
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Microglia / metabolism
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Obesity / drug therapy*
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Obesity / metabolism
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Palmitic Acid / metabolism
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Palmitic Acid / pharmacology
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Polyphenols / pharmacology
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STAT3 Transcription Factor / metabolism
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Tea / metabolism
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Anti-Obesity Agents
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Interleukin-1beta
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Interleukin-6
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Polyphenols
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STAT3 Transcription Factor
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Tea
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Tumor Necrosis Factor-alpha
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Palmitic Acid
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Catechin
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epigallocatechin gallate
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Janus Kinase 2