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Estrogen‐mediated protection against methamphetamine‐induced inflammatory pathways in human brain endothelial cells
Author(s) -
Lee Y. W.,
Małecki A.,
Toborek M.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.85.s2.22_10.x
Subject(s) - meth , methamphetamine , estrogen , creb , pharmacology , transcription factor , signal transduction , human brain , inflammation , cancer research , chemistry , microbiology and biotechnology , medicine , biology , neuroscience , gene , biochemistry , monomer , organic chemistry , acrylate , polymer
Recent evidence has demonstrated the potential role of estrogens as therapeutic agents in the prevention or treatment of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease or stroke. The present study focused on the protective mechanisms of estrogens in the methamphetamine (METH)‐mediated inflammatory reactions in human brain microvascular endothelial cells (HBMEC). Pretreatment with estrogens markedly blocked the activation of redox‐responsive transcription factors, such as AP‐1, NF‐kappaB and CREB, in HBMEC exposed to METH. In addition, estrogens inhibited METH‐induced expression of inflammatory genes in HBMEC. These results suggest that estrogens may attenuate the METH‐induced inflammatory cerebrovascular environments via blocking the transcription factor‐mediated molecular signaling pathways in human brain endothelial cells. Acknowledgements: Supported by NIH; NS39254, MH63022, and AA013843.