Neuroinflammation and endoplasmic reticulum stress are coregulated by cyclo(His-Pro) to prevent LPS neurotoxicity
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- 作者：Ilaria Bellezzaa ; ilaria.bellezza@unipg.it" class="auth_mail ; Silvia Grottellia ; Anna Lisa Mierlaa ; Ivana Cacciatoreb ; Erika Fornasarib ; Luca Roscinic ; Gianluigi Cardinalic ; Alba Minellia
- 关键词：AD ; Alzheimer's disease ; AIDS ; acquired immune deficiency syndrome ; ALS ; amyotrophic lateral sclerosis ; Ara C ; (尾-d-Arabinofuranosyl)cytosin ; Bip ; binding immunoglobulin protein/78  ; kDa glucose-regulated protein ; CCM ; cell conditioned medium ; CHOP ; C/EBP-homologous protein ; CHP ; cyclo-(His-Pro) ; CNS ; central nervous system ; COX-2 ; cyclooxygenase ; DCFH-DA ; 2&prime ; 7&prime ; -dichlorofluorescein-diacetate ; eIF2伪 ; eukaryotic translation initiation factor 2 ; EpRE/ARE ; electrophile/antioxidant res
- 刊名：The International Journal of Biochemistry and Cell Biology
- 出版年：June 2014
- 年：2014
- 卷：51
- 期：Complete
- 页码：159-169
- 全文大小：2581 K
文摘
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Cyclo(His-Pro) presides over the Nrf2–NF-魏B systems in LPS-activated BV-2.
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Cyclo(His-Pro) attenuates endoplasmic reticulum stress in BV-2 cells.
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Cyclo(His-Pro) reduces pro-inflammatory cytokine release by BV-2.
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Cyclo(His-Pro) reduces glial inflammation after systemic LPS administration.