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Inflammation

, Volume 39, Issue 6, pp 1904–1917 | Cite as

Paeonol Suppresses Neuroinflammatory Responses in LPS-Activated Microglia Cells

  • Li Xia He
  • Xiaoyun Tong
  • Jing Zeng
  • Yuanqing Tu
  • Saicun Wu
  • Manping Li
  • Huaming Deng
  • Miaomiao Zhu
  • Xiucun Li
  • Hong Nie
  • Li YangEmail author
  • Feng HuangEmail author
ORIGINAL ARTICLE

Abstract

In this work, we assessed the anti-inflammatory effects of paeonol (PAE) in LPS-activated N9 microglia cells, as well as its underlying molecular mechanisms. PAE had no adverse effect on the viability of murine microglia N9 cell line within a broad range (0.12∼75 μM). When N9 cell line was activated by LPS, PAE (0.6, 3, 15 μM) significantly suppressed the release of proinflammatory products, such as nitric oxide (NO), interleukin-1β (IL-1β), and prostaglandin E2 (PGE2), demonstrated by the ELISA assay. Moreover, the levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were significantly reduced in PAE-treated N9 microglia cells. We also examined some proteins involved in immune signaling pathways and found that PAE treatment significantly decreased the expression of TLR4, MyD88, IRAK4, TNFR-associated factor 6 (TRAF6), p-IkB-α, and NF-kB p65, as well as the mitogen-activated protein kinase (MAPK) pathway molecules p-P38, p-JNK, and p-ERK, indicating that PAE might act on these signaling pathways to inhibit inflammatory responses. Overall, we found that PAE had anti-inflammatory effect on LPS-activated N9 microglia cells, possibly via inhibiting the TLR4 signaling pathway, and it could be a potential drug therapy for inflammation-associated neurodegenerative diseases.

KEY WORDS

anti-inflammatory neurodegenerative disease paeonol microglia cells 

Notes

Acknowledgments

This work was supported by the Medical Scientific Research Foundation of Guangdong Province (No. A2010344), the 211 Project, and the Key Laboratory of Innovative Research Projects of the College of Pharmacy of Jinan University.

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© Springer Science+Business Media New York 2016

Authors and Affiliations

  1. 1.Department of Traditional Chinese Medicine, College of PharmacyJinan UniversityGuangzhouChina
  2. 2.The First Affiliated Hospital of Yunnan University of Traditional Chinese MedicineKunmingChina
  3. 3.Department of Molecular Pharmacology, School of Traditional Chinese Materia MedicaYunnan University of Traditional Chinese MedicineKunmingChina

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