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  • br Acknowledgements This work was supported by the FedEx Ins

    2024-07-10


    Acknowledgements This work was supported by the FedEx Institute of Technology at The University of Memphis (to DLB and ALP), NSF REU CHE 1156738 (to ALP in support of RSS), and NIHCA921060 (to GT). This material is based upon work supported by the National Science Foundation under Grant No. CHE-1531466. Thanks also to the Chemical Computing Group, Montreal, Canada for the Molecular Operating Environment (MOE). We thank Dr. Roberto de la Salud Bea from Rhodes College for synthesis advice. We also thank Daniel Hoagland and Dr. Richard Lee from St. Jude Children’s Research Hospital for purity testing of 22.
    Free radicals are a normal product of cellular oxygen metabolism in mammals and are central players in the physiological control of cellular function . However, in certain situations, free radical-associated damage occurs, which may be an important factor in many pathological processes . The incidence of neurodegenerative diseases has dramatically risen over the past several decades; many of these diseases, such as Alzheimer or Parkinson disease, are accompanied by the accumulation of oxidized proteins. The human Epiandrosterone is particularly exposed to oxidative stress, at least in part because of its high oxygen consumption. Glial cells are essential to assist, protect, and support neuron physiology. Microglia cells are the nervous system equivalent of monocytes–macrophages and constitute a key element of the immune response in the brain. At inflammation sites, activated microglial cells produce high levels of free radicals, such as NO, as well as proinflammatory cytokines, which can be found at abnormal levels in affected regions of the nervous system in pathological situations, for example, multiple sclerosis, Alzheimer disease, and Parkinson disease . Autotaxin (ATX) was first identified as a cancer cell motility factor, but was recently discovered to possess lysophospholipase D activity, and it converts lysophospholipids such as lysophosphatidylcholine to lysophosphatidic acid (LPA) , . Recent reports indicate that ATX plays a role in the progression of inflammatory-associated pathologies. ATX expression is increased at the protein level in the cerebrospinal fluid of multiple sclerosis patients and at the mRNA level in the frontal cortex of Alzheimer-type dementia patients . In adipose tissues, ATX mRNA was found to be increased during adipocyte differentiation and was up-regulated in genetically obese diabetic mice (db/db) . The surface expression of LPA receptors (LPAR1) on microglia is now well established . However, despite the fact that microglial activation is widely considered to be a hallmark of neurodegenerative disorders, the importance of ATX expression by microglia under oxidative stress conditions remains unclear.