Anti-inflammatory Effects of Curcumin in Microglial Cells

Lipoteichoic acid (LTA) induces neuroinflammatory molecules, contributing to the pathogenesis of neurodegenerative diseases. Therefore, suppression of neuroinflammatory molecules could be developed as a therapeutic method. Although previous data supports an immune-modulating effect of curcumin, the...

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Main Authors: Yangyang Yu, Qian Shen, Yihong Lai, Sun Y. Park, Xingmei Ou, Dongxu Lin, Meiling Jin, Weizhen Zhang
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-04-01
Series:Frontiers in Pharmacology
Subjects:
Online Access:http://journal.frontiersin.org/article/10.3389/fphar.2018.00386/full
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author Yangyang Yu
Qian Shen
Yihong Lai
Sun Y. Park
Xingmei Ou
Dongxu Lin
Meiling Jin
Weizhen Zhang
author_facet Yangyang Yu
Qian Shen
Yihong Lai
Sun Y. Park
Xingmei Ou
Dongxu Lin
Meiling Jin
Weizhen Zhang
author_sort Yangyang Yu
collection DOAJ
description Lipoteichoic acid (LTA) induces neuroinflammatory molecules, contributing to the pathogenesis of neurodegenerative diseases. Therefore, suppression of neuroinflammatory molecules could be developed as a therapeutic method. Although previous data supports an immune-modulating effect of curcumin, the underlying signaling pathways are largely unidentified. Here, we investigated curcumin’s anti-neuroinflammatory properties in LTA-stimulated BV-2 microglial cells. Inflammatory cytokine tumor necrosis factor-α [TNF-α, prostaglandin E2 (PGE2), and Nitric Oxide (NO] secretion in LTA-induced microglial cells were inhibited by curcumin. Curcumin also inhibited LTA-induced inducible NO synthases (iNOS) and cyclooxygenase-2 (COX-2) expression. Subsequently, our mechanistic studies revealed that curcumin inhibited LTA-induced phosphorylation of mitogen-activated protein kinase (MAPK) including ERK, p38, Akt and translocation of NF-κB. Furthermore, curcumin induced hemeoxygenase (HO)-1HO-1 and nuclear factor erythroid 2-related factor 2 (Nrf-2) expression in microglial cells. Inhibition of HO-1 reversed the inhibition effect of HO-1 on inflammatory mediators release in LTA-stimulated microglial cells. Taken together, our results suggest that curcumin could be a potential therapeutic agent for the treatment of neurodegenerative disorders via suppressing neuroinflammatory responses.
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spelling doaj.art-fb2d3d31ac2446068624afc3a0ca1aa02022-12-22T01:08:16ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122018-04-01910.3389/fphar.2018.00386345045Anti-inflammatory Effects of Curcumin in Microglial CellsYangyang Yu0Qian Shen1Yihong Lai2Sun Y. Park3Xingmei Ou4Dongxu Lin5Meiling Jin6Weizhen Zhang7Shenzhen University Health Science Center, Shenzhen, ChinaShenzhen University Health Science Center, Shenzhen, ChinaShenzhen University Health Science Center, Shenzhen, ChinaBio-IT Fusion Technology Research Institute, Pusan National University, Busan, South KoreaShenzhen University Health Science Center, Shenzhen, ChinaShenzhen University Health Science Center, Shenzhen, ChinaShenzhen University Health Science Center, Shenzhen, ChinaShenzhen University Health Science Center, Shenzhen, ChinaLipoteichoic acid (LTA) induces neuroinflammatory molecules, contributing to the pathogenesis of neurodegenerative diseases. Therefore, suppression of neuroinflammatory molecules could be developed as a therapeutic method. Although previous data supports an immune-modulating effect of curcumin, the underlying signaling pathways are largely unidentified. Here, we investigated curcumin’s anti-neuroinflammatory properties in LTA-stimulated BV-2 microglial cells. Inflammatory cytokine tumor necrosis factor-α [TNF-α, prostaglandin E2 (PGE2), and Nitric Oxide (NO] secretion in LTA-induced microglial cells were inhibited by curcumin. Curcumin also inhibited LTA-induced inducible NO synthases (iNOS) and cyclooxygenase-2 (COX-2) expression. Subsequently, our mechanistic studies revealed that curcumin inhibited LTA-induced phosphorylation of mitogen-activated protein kinase (MAPK) including ERK, p38, Akt and translocation of NF-κB. Furthermore, curcumin induced hemeoxygenase (HO)-1HO-1 and nuclear factor erythroid 2-related factor 2 (Nrf-2) expression in microglial cells. Inhibition of HO-1 reversed the inhibition effect of HO-1 on inflammatory mediators release in LTA-stimulated microglial cells. Taken together, our results suggest that curcumin could be a potential therapeutic agent for the treatment of neurodegenerative disorders via suppressing neuroinflammatory responses.http://journal.frontiersin.org/article/10.3389/fphar.2018.00386/fullcurcuminneuroinflammationTLR2HO-1microglial cells
spellingShingle Yangyang Yu
Qian Shen
Yihong Lai
Sun Y. Park
Xingmei Ou
Dongxu Lin
Meiling Jin
Weizhen Zhang
Anti-inflammatory Effects of Curcumin in Microglial Cells
Frontiers in Pharmacology
curcumin
neuroinflammation
TLR2
HO-1
microglial cells
title Anti-inflammatory Effects of Curcumin in Microglial Cells
title_full Anti-inflammatory Effects of Curcumin in Microglial Cells
title_fullStr Anti-inflammatory Effects of Curcumin in Microglial Cells
title_full_unstemmed Anti-inflammatory Effects of Curcumin in Microglial Cells
title_short Anti-inflammatory Effects of Curcumin in Microglial Cells
title_sort anti inflammatory effects of curcumin in microglial cells
topic curcumin
neuroinflammation
TLR2
HO-1
microglial cells
url http://journal.frontiersin.org/article/10.3389/fphar.2018.00386/full
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AT xingmeiou antiinflammatoryeffectsofcurcumininmicroglialcells
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AT meilingjin antiinflammatoryeffectsofcurcumininmicroglialcells
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