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Anthocyanins Downregulate Lipopolysaccharide-Induced Inflammatory Responses in BV2 Microglial Cells by Suppressing the NF-κB and Akt/MAPKs Signaling Pathways
Department of Biochemistry, Dongeui University College of Oriental Medicine, Busan 614-052, Korea
Anti-Aging Research Center & Blue-Bio Industry RIC, Dongeui University, Busan 614-714, Korea
Department of Internal Medicine, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 660-702, Korea
Gyeongnam Regional Cancer Center, Gyeongsang National University Hospital, Jinju 660-702, Korea
Department of Chemistry, Research Institute of Life Science, Gyeongsang National University, Jinju 660-701, Korea
Faculty of Applied Marine Science, Cheju National University, Jeju 690-756, Korea
Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Yangsan 626-870, Korea
* Authors to whom correspondence should be addressed.
Received: 12 December 2012; in revised form: 1 January 2013 / Accepted: 7 January 2013 / Published: 14 January 2013
Abstract: Anthocyanins are naturally occurring polyphenols that impart bright color to fruits, vegetables and plants and have a variety of protective properties, which have generally been attributed to their antioxidant capacity. However, little is known about the molecular mechanisms underlying anti-inflammatory effects of anthocyanins related to neurodegenerative diseases. Therefore, we determined whether anthocyanins isolated from black soybean seed coats would inhibit pro-inflammatory mediators and cytokines in lipopolysaccharide (LPS)-stimulated murine BV2 microglial cells. Our results showed that anthocyanins significantly inhibited LPS-induced pro-inflammatory mediators, such as nitric oxide (NO) and prostaglandin E2, and pro-inflammatory cytokines including tumor necrosis factor (TNF)-α and interleukin (IL)-1β, without significant cytotoxicity. Anthocyanins also downregulated excessive expression of inducible NO synthase, cyclooxygenase-2, TNF-α, and IL-1β in LPS-stimulated BV2 cells. Moreover, anthocyanins inhibited nuclear translocation of nuclear factor-kappa B (NF-κB) by reducing inhibitor of NF-κB alpha degradation as well as phosphorylating extracellular signal-regulated kinase, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase, and Akt. These findings suggest that anthocyanins may offer substantial therapeutic potential for treating inflammatory and neurodegenerative diseases accompanied by microglial activation.
Keywords: anthocyanins; BV2; anti-inflammatory activity; NF-κB; MAPK; Akt
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Cite This Article
MDPI and ACS Style
Jeong, J.-W.; Lee, W.S.; Shin, S.C.; Kim, G.-Y.; Choi, B.T.; Choi, Y.H. Anthocyanins Downregulate Lipopolysaccharide-Induced Inflammatory Responses in BV2 Microglial Cells by Suppressing the NF-κB and Akt/MAPKs Signaling Pathways. Int. J. Mol. Sci. 2013, 14, 1502-1515.
Jeong J-W, Lee WS, Shin SC, Kim G-Y, Choi BT, Choi YH. Anthocyanins Downregulate Lipopolysaccharide-Induced Inflammatory Responses in BV2 Microglial Cells by Suppressing the NF-κB and Akt/MAPKs Signaling Pathways. International Journal of Molecular Sciences. 2013; 14(1):1502-1515.
Jeong, Jin-Woo; Lee, Won S.; Shin, Sung C.; Kim, Gi-Young; Choi, Byung T.; Choi, Yung H. 2013. "Anthocyanins Downregulate Lipopolysaccharide-Induced Inflammatory Responses in BV2 Microglial Cells by Suppressing the NF-κB and Akt/MAPKs Signaling Pathways." Int. J. Mol. Sci. 14, no. 1: 1502-1515.