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Presently, the effects of 6\u2010OHDA on endothelial dysfunction remain unknown. Using a 6\u2010OHDA rodent model of PD, we found that administration of 6\u2010OHDA could increase the expression of endothelial adhesion molecules, such as intercellular adhesion molecule 1 (ICAM\u20101), vascular cell adhesion molecule 1 (VCAM\u20101), and E\u2010selectin. An <jats:italic>in vitro<\/jats:italic> study displayed that treatment with 6\u2010OHDA increased the release of these molecules in human brain microvascular endothelial cells in a dose\u2010dependent manner. Correspondingly, 6\u2010OHDA significantly increased attachment of THP\u20101 monocytes to brain endothelial cells. In addition, real\u2010time polymerase chain reaction and enzyme\u2010linked immunosorbent assay results indicated that 6\u2010OHDA elevated the production of proinflammatory cytokines, such as interleukin\u20101\u03b2, interleukin\u20106, and tumor necrosis factor\u2010\u03b1. Furthermore, 6\u2010OHDA treatment increased the expression of cyclooxygenase\u20102 and inducible nitric oxide synthase, as well as the production of prostaglandin E2 and nitric oxide. Importantly, 6\u2010OHDA elevated the transcriptional activity of NF\u2010\u043aB by increasing the phosphorylation, degradation, and subsequent nuclear translocation of p65. Mechanistically, the angiotensin II type 1 receptor was found to mediate 6\u2010OHDA\u2010induced endothelial dysfunction. Our findings suggest that 6\u2010OHDA\u2010induced endothelial inflammation may play an important role in the pathogenesis of PD. \u00a9 2017 IUBMB Life, 69(11):887\u2013895, 2017<\/jats:p>","DOI":"10.1002\/iub.1685","type":"journal-article","created":{"date-parts":[[2017,10,19]],"date-time":"2017-10-19T12:16:45Z","timestamp":1508415405000},"page":"887-895","source":"Crossref","is-referenced-by-count":18,"title":["6\u2010Hydroxydopamine induces brain vascular endothelial inflammation"],"prefix":"10.1002","volume":"69","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8738-0250","authenticated-orcid":false,"given":"Qizhi","family":"Fu","sequence":"first","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology Luoyang Henan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Runluo","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology Luoyang Henan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongxi","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery The First Hospital of Jilin University Changchun Jilin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi","family":"Shan","sequence":"additional","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology Luoyang Henan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenna","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology Luoyang Henan China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,10,19]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/neup.12262"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms141122163"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF03033565"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.3389\/fnana.2014.00155"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2009.06189.x"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2016.09.013"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2016.09.004"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1002\/ana.20369"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1750-3639.2012.00628.x"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1042\/BST20140319"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1006\/exmp.2001.2368"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00395-005-0511-6"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms150711324"},{"key":"e_1_2_7_15_1","first-page":"8","article-title":"Neurovascular dysfunction, inflammation and endothelial activation: implications for the pathogenesis of Alzheimer's disease","volume":"25","author":"Grammas P.","year":"2011","journal-title":"J. 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