Minocycline suppresses hypoxic activation of rodent microglia in culture☆
Section snippets
Acknowledgements
This work was supported by grants from the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (03-PJ1-PG10-21300-0011).
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2019, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :Hypoxia induces directly microglial activation (Suk, 2004; Wang and Wang, 2007; J.J. Li et al., 2008; Li et al., 2009; Pardo-Peña et al., 2018) and changes in microglial morphology (You and Kaur, 2000; Deng et al., 2008, 2009; Fig. 2), proliferation rate (Deng et al., 2009), phagocytic activity (Deng et al., 2008), production of proinflammatory enzymes (You and Kaur, 2000) and inflammatory mediators such as NO, IL-1β, IL-6, TNF-α, ROS and PGE2 in an inflammasome-dependent manner (Suk, 2004; Deng et al., 2008, 2010, 2011; Smith et al., 2013; Liu et al., 2017; Pardo-Peña et al., 2018; Silva et al., 2018). Most of these effects on microglia are also observed in microglial cell lines (F. Li et al., 2008) and are inhibited by minocycline (Suk, 2004; Pardo-Peña et al., 2018; Silva et al., 2018). Moreover, acute hypoxia increases LPS effects on cultured microglia and potentiates iNOS, TNF-α and NF-κB expression (Guo and Bhat, 2006), clearly indicating that hypoxia induces a proinflammatory state through microglial activation.
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Supplementary data associated with this article can be found at doi:10.1016/j.neulet.2004.05.038.