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Oxidative Stress and Inflammation
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Varsha Rana, Dey Parama, Sosmitha Girisa, Choudhary Harsha, Ajaikumar B. Kunnumakkara
Microglia are macrophagic cells located throughout the brain and spinal cord. Under normal conditions, they exhibit a resting phenotype. However, when the brain encounters any damage or infection, conserved structural motifs such as the danger-associated molecular patterns or DAMPs (from damaged or stressed tissues during brain injury) and the pathogen-associated molecular patterns or PAMPs (from pathogens, during infection) bind to the toll-like receptors (TLRs). This binding results in microglial activation and mediates the release of pro-inflammatory cytokines, ROS, etc. Prolonged microglial activation provokes inflammation and further augments the neuronal damage eventually leading to neurodegeneration. Thus, microglial activation plays a critical role as an initiator during inflammation-mediated neuronal injury (Amor et al., 2010; Spangenberg and Green, 2017; Zhang et al., 2018b). The NLRP3 inflammasome signaling pathway activation-mediated by oxidative stress in microglia is crucial for the development and progression of various neurodegenerative diseases (Lang et al., 2018). A study conducted by Bai et al. (2018) demonstrated that the reactive species H2O2 induced the release of IL-1β by activating cathepsin B (CTSB), which subsequently activated the NLRP3 inflammasome signaling pathway in microglia.
The Opioid Epidemic
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Glial cells play an important role in creating a neuroinflammatory state. As non-neuronal cells inhabiting the central nervous system and peripheral nervous system, glial cells play a supportive role in maintenance and regulation. Glial cells include oligodendrocytes, astrocytes, ependymal cells, and microglia in the central nervous system. Schwann cells and satellite cells support the peripheral nervous system. Microglia cells are particularly important and serve as resident macrophages in the brain and spinal cord, and as such are active against damaged neurons and infectious agents. At rest, microglia do not typically contribute to the synaptic milieu of neurotransmitters. This is in contrast to astrocytes which play an active function in taking up and releasing neurotransmitters.
Pathophysiology of Spinal Shock
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Siobhán M. Hartigan, Elizabeth A. Rourke, Roger R. Dmochowski
Historically, neuroinflammation was frequently viewed as deleterious to neurologic function and recovery following SCI, as it was previously thought that suppression of immune response would be neuroprotective; however, recent studies have revealed some beneficial aspects of inflammation that should not be inhibited.29,30 Microglia and infiltrating macrophages in the CNS are heterogenous, with diverse functions that range from pro-inflammatory (M1-like) phenotypes to immunosuppressive (M2-like) phenotypes.31 Microglia are the primary mediators of the innate immune response in the CNS and play a critical role in neuroinflammation and secondary injury following injury to the CNS, such as SCI. Inflammatory response following SCI for wound healing also includes leukocyte influx from the periphery, lesion debris clearance by neutrophils, tissue remodeling, axonal regrowth, and remyelination.32 In order to develop therapeutic methods of modulating the immune system, further work needs to be conducted to better understand immune cell subtypes that are more detrimental than beneficial and those that are necessary in repair.
Neuroinflammation after ischemic stroke involves INPP5D expression mediated by the TMPO-AS1-PU.1 complex
Published in Neurological Research, 2023
Wenhui Luan, Zhongwen Sun, Chunmei Wu, Manli Tao, Xiaoqian Shen
According to statistics from the Global Burden of Disease, Injury and Risk Factors Study (GBD), stroke is a disease with a high mortality and disability rate worldwide [1]. It is estimated that 6 million people die from stroke each year, and there are 2.5 million new cases in China each year [2]. As the most common stroke subtype, ischemic stroke (IS) accounts for approximately 85% of all stroke cases [3]. Microglia are resident immune cells in the brain, accounting for 10–15% of central nervous system (CNS) cells. Microglia are activated immediately after cerebral ischemia, which are involved in tissue damage [4]. ‘Activated’ microglia usually have antigen presentation and killing effects, and secrete a variety of inflammatory factors to cause a strong inflammatory response. Inducible nitric oxide synthase (iNOS) is a commonly used marker of ‘activated’ microglia. In contrast, ‘resting’ microglia enhance phagocytic activity to remove debris and produce many anti-inflammatory factors. And arginase 1 (Arg1) is one of the best markers for ‘resting’ microglia [5]. In fact, this binary classification is too simplistic, because there are many overlapping functional states of microglia. Microglia could promote damage or promote repair, depending on the activation signal they receive [6].
Jing-an oral liquid alleviates Tourette syndrome via the NMDAR/MAPK/CREB pathway in vivo and in vitro
Published in Pharmaceutical Biology, 2022
Leying Xi, Xixi Ji, Wenxiu Ji, Yue’e Yang, Yajie Zhang, Hongyan Long
Microglia are the resident immune cells of the CNS. Abnormally activated microglia secrete high levels of amino acids, which can result in neurological damage. CD11b and IBa1 are the signature proteins of microglia. The binding neurotransmitters to receptors are important for activation downstream signaling pathway. Over the last decade, there has been increasing evidence that microglia can express various functional GluRs, including α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, kainite, and NMDARs (Murugan et al. 2013). Furthermore, it was observed in another study that MK801 (a non-competitive NMDAR antagonist) inhibits LPS-induced microglia activation (Thomas and Kuhn 2005). The expression of functional GluRs is evident in microglia, and GluR activation is known to be associated with Glu release, cytokine release, microglia activation, and nitric oxide production (Byrnes et al. 2009; Murugan et al. 2011; Beppu et al. 2013). Therefore, GluRs on microglia may be a therapeutic target for neurological disorders involving microglia activation.
Carnosol suppresses microglia cell inflammation and apoptosis through PI3K/AKT/mTOR signaling pathway
Published in Immunopharmacology and Immunotoxicology, 2022
Yuhan Yan, Yu Liu, Yujiao Yang, Yi Ding, Xin Sun
Microglia are the main immune cells in the central nervous system and participate in the pathological process of nerve injury by secreting inflammatory and presenting antigen [19]. The activity of microglia is the basis for their biological functions. When microglia apoptosis occurs, it will reduce the ability of the body's brain to resist microbial infection. On the other hand, apoptotic microglia also release a large number of cytokines, including inflammatory factors, which further aggravate the body's brain damage [20,21]. Therefore, to inhibit the apoptosis of microglia is of great significance to enhance the anti-infection ability of brain tissue and alleviate ischemic cerebrovascular diseases. Zhou et al. [22] demonstrated that Ginkgo extracts play a neuroprotection effect via promoting the cell viability and suppressing the apoptosis rates of the OGD/R treated BV2 cells. In this study, carnosol alleviated the accumulation of oxidative stress and inflammation response, promoted the proliferation and inhibited the apoptosis rate of the OGD treated BV2 cells, implying carnosol relieved ischemic stroke via restoring the cellular functions of BV2 cells.