Research Article Amelioration of LPS-Induced Inflammation Response in Microglia by AMPK Activation Chin-Chen Chen, 1 Jiun-Tsai Lin, 2 Yi-Fang Cheng, 2 Cheng-Yi Kuo, 2 Chun-Fang Huang, 2 Shao-Hsuan Kao, 3 Yao-Jen Liang, 1,4 Ching-Yi Cheng, 5 and Han-Min Chen 1,2,4 1 Institute of Applied Science and Engineering, Catholic Fu-Jen University, New Taipei City 24205, Taiwan 2 Energenesis Biomedical Co., Ltd., New Taipei City 24205, Taiwan 3 Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung City 40201, Taiwan 4 Department of Life Science, Catholic Fu-Jen University, New Taipei City 24205, Taiwan 5 Research Center for Industry of Human Ecology, Graduate Institute of Health Industry Technology, Department of Cosmetic Science, Chang Gung University of Science and Technology, Taoyuan 33303, Taiwan Correspondence should be addressed to Han-Min Chen; steven@energenesis-biomedical.com Received 31 March 2014; Revised 22 May 2014; Accepted 30 May 2014; Published 17 June 2014 Academic Editor: Nicole Clarke Copyright © 2014 Chin-Chen Chen et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Adenosine 5  -monophosphate-activated protein kinase (AMPK) is a key regulator of cellular energy homeostasis via modulating metabolism of glucose, lipid, and protein. In addition to energy modulation, AMPK has been demonstrated to associate with several important cellular events including infammation. Te results showed that ENERGI-F704 identifed from bamboo shoot extract was nontoxic in concentrations up to 80 M and dose-dependently induced phosphorylation of AMPK (Tr-172) in microglia BV2 cells. Our fndings also showed that the treatment of BV2 with ENERGI-F704 ameliorated the LPS-induced elevation of IL-6 and TNF- production. In addition, ENERGI-F704 reduced increased production of nitric oxide (NO) and prostaglandin E2 (PGE2) via downregulating the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2), respectively. Moreover, ENERGI-F704 decreased activated nuclear translocation and protein level of NF-B. Inhibition of AMPK with compound C restored decreased NF-B translocation by ENERGI-F704. In conclusion, ENERGI-F704 exerts inhibitory activity on LPS-induced infammation through manipulating AMPK signaling and exhibits a potential therapeutic agent for neuroinfammatory disease. 1. Introduction Homeostasis of proinfammatory and anti-infammatory response in brain is shifed towards a proinfammatory state with age, so neuroinfammation has been implicated as an important etiological factor in several aging-related neurode- generative diseases, such as Alzheimer’s disease and Parkin- son’s disease [1–3]. Due to the involvement of infammation in pathogenesis, many studies were devoted to the therapy of neurodegenerative diseases using anti-infammatory strate- gies [4]. Microglia are myeloid-lineage cells residing in the central nervous system. As a neuron protector, microglia are sensitive to microenvironment and readily become activated in response to immunological stimuli, toxin, or injury [5]. Upon activation, however, microglia secrete a variety of proinfammatory cytokines or other cytotoxic factors, which are believed to exacerbate neurodegeneration. It has been reported that lipopolysaccharides (LPS) and/or interferon- enhanced the production of NO in microglia via inducible nitric oxide synthase (iNOS) and caused neuron death within 48 hours [6]. In addition, the increased proinfammatory cytokines such as TNF-, IL-1, and IL-6 in either cell culture or animal models induce neuron degeneration [7–12]. NF-B, a transcriptional factor, regulates several proin- fammatory cytokines and infammation-related protein expression such as TNF-, IL-1, IL-6, COX-2, and iNOS [13]. Upon stimulation, activated IB kinase (IKK) phos- phorylates IB, which results in the dissociation of NF-B- IB complex and thereby translocation of active NF-B into nucleus. Activation of NF-B has been found in several Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 692061, 9 pages http://dx.doi.org/10.1155/2014/692061