4.5 Article

Anti-neuroinflammatory Effect of Emodin in LPS-Stimulated Microglia: Involvement of AMPK/Nrf2 Activation

期刊

NEUROCHEMICAL RESEARCH
卷 41, 期 11, 页码 2981-2992

出版社

SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-016-2018-6

关键词

Microglia; Emodin; Anti-neuroinflammation; AMPK; Nrf2

资金

  1. Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education, Science, and Technology [2015R1D1A1A01059450]
  2. High Value-added Food Technology Development Program, Ministry for Food, Agriculture, Forestry and Fisheries, Republic of Korea [314043-03-1-HD020]
  3. National Research Foundation of Korea [2015R1D1A1A01059450] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

AMPK/Nrf2 signaling regulates multiple antioxidative factors and exerts neuroprotective effects. Emodin is one of the main bioactive components extracted from Polygonum multiflorum, a plant possessing important activities for human health and for treating a variety of diseases. This study examined whether emodin can activate AMPK/Nrf2 signaling and induce the expression of genes targeted by this pathway. In addition, the anti-neuroinflammatory properties of emodin in lipopolysaccharide (LPS)-stimulated microglia were examined. In microglia, the emodin treatment increased the levels of LKB1, CaMKII, and AMPK phosphorylation. Emodin increased the translocation and transactivity of Nrf2 and enhanced the levels of HO-1 and NQO1. In addition, the emodin-mediated expression of HO-1 and NQO1 was attenuated completely by an AMPK inhibitor (compound C). Moreover, emodin decreased dramatically the LPS-induced production of NO and PGE(2) as well as the protein expression and promoter activity of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). In addition, emodin effectively inhibited the production of pro-inflammatory cytokines, TNF-alpha and IL-6, and reduced the level of I kappa B alpha phosphorylation, leading to the suppression of the nuclear translocation, phosphorylation, and transactivity of NF-kappa B. Emodin also suppressed the LPS-stimulated activation of STATs, JNK, and p38 MAPK. The anti-inflammatory effects of emodin were reversed by transfection with Nrf-2 and HO-1 siRNA and by a co-treatment with an AMPK inhibitor. These results suggest that emodin isolated from P. multiflorum can be used as a natural anti-neuroinflammatory agent that exerts its effects by inducing HO-1 and NQO1 via AMPK/Nrf2 signaling in microglia.

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