title: Expression of angiotensin II and its receptors in activated microglia in experimentally induced cerebral ischemia in the adult rats.
abstract: Expression of angiotensin II (Ang II) and its receptors (AT1/AT2) is undetected in the mature microglia in normal brain. We report here that the immunoexpression of Ang II and AT1/AT2 was altered in activated microglia notably at 1 week in rats subjected to middle cerebral artery occlusion (MCAO). Immunolabeled activated microglia were widely distributed in the infarcted cerebral tissue after MCAO. By enzyme immunoassay, Ang II protein expression levels of the ischemic tissues were decreased drastically at 12 h after ischemia, then rose rapidly at 3 days and 1 week after MCAO when compared with the control. On the other hand, AT1 and AT2 receptor mRNA and protein levels were up-regulated after MCAO, peaking at 12 h, but declined thereafter. Expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) mRNA and protein levels was concomitantly increased. Edaravone significantly suppressed Ang II and AT1/AT2 receptor expression as well as that of TNF-α and IL-1β suggesting that microglia-derived Ang II can act through an autocrine manner via its receptor that may be linked partly to the production of proinflammatory cytokines. We conclude that neuroinflammation in MCAO may be attenuated by Edaravone which acts through suppression of expression of Ang II and its receptors and proinflammatory cytokines in activated microglia.
authors.affiliation: Department of Histology and Embryology, Faculty of Basic Medical Sciences, Kunming Medical University, 1168 West Chunrong Road, Kunming, 650500, People's Republic of China.
authors.forename: Chun-Yun
authors.initials: CY
authors.lastname: Wu
authors.forename: Hao
authors.initials: H
authors.lastname: Zha
authors.forename: Qing-Qing
authors.initials: QQ
authors.lastname: Xia
authors.forename: Yun
authors.initials: Y
authors.lastname: Yuan
authors.forename: Xiao-Yan
authors.initials: XY
authors.lastname: Liang
authors.forename: Jing-Hui
authors.initials: JH
authors.lastname: Li
authors.forename: Ze-Yun
authors.initials: ZY
authors.lastname: Guo
authors.forename: Juan-Juan
authors.initials: JJ
authors.lastname: Li
mesh_terms: D000375:Aging / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D000983:Antipyrine / Q000031:analogs & derivatives / Q000494:pharmacology; D015153:Blotting, Western; D002545:Brain Ischemia / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D000077553:Edaravone; D005786:Gene Expression Regulation / Q000187:drug effects; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008297:Male; D017628:Microglia / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D021381:Protein Transport / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics / Q000378:metabolism*; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D014409:Tumor Necrosis Factor-alpha; D000804:Angiotensin II; D000077553:Edaravone; D000983:Antipyrine