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Src-suppressed C kinase substrates (SSeCKS), a substrate of protein kinase C, plays an important role in maintaining cell junctions and cell morphology and regulating cell permeability. However, whether DHA can increase SSeCKS expression and then mediate the Ang-1\/Ang-2 ratio still needs to be studied. Human cerebrovascular pericytes (HBVPs) cultured in vitro were divided into groups, treated with or without DHA along with SSeCKS siRNA to knockdown SSeCKS expression, and then subjected to 24\u00a0h of hypoxia followed by 6\u00a0h of reoxygenation. Cell viability; lactate dehydrogenase (LDH) release; and Ang-1, Ang-2 and VEGF activity were detected by using ELISA kits. The apoptosis rate was assessed by TUNEL flow cytometry. Expression of the SSeCKS, Ang-1, Ang-2 and VEGF proteins was evaluated by western blotting. Pretreatment with 10\u00a0\u03bcM or 40\u00a0\u03bcM DHA efficiently attenuated hypoxia\/reoxygenation (H\/R) injury by activating SSeCKS to increase the Ang-1\/Ang-2 ratio and downregulate VEGF expression in HBVPs, as evidenced by decreased LDH release and apoptotic rates and increased HBVPs viability. Meanwhile, after we used SSeCKS siRNA to knock down SSeCKS protein expression, the protective effect of DHA on HBVPs following H\/R injury was reversed. In conclusion, DHA can activate SSeCKS to increase the Ang-1\/Ang-2 ratio and downregulate VEGF expression in HBVPs, thus reducing H\/R injury.<\/jats:p>","DOI":"10.1007\/s11064-019-02915-0","type":"journal-article","created":{"date-parts":[[2019,11,27]],"date-time":"2019-11-27T11:03:16Z","timestamp":1574852596000},"page":"310-321","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["DHA Attenuates Hypoxia\/Reoxygenation Injury by Activating SSeCKS in Human Cerebrovascular Pericytes"],"prefix":"10.1007","volume":"45","author":[{"given":"Yanli","family":"Yu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haibin","family":"Fang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhen","family":"Qiu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongyuan","family":"Xia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2019,11,27]]},"reference":[{"issue":"2","key":"2915_CR1","doi-asserted-by":"publisher","first-page":"144","DOI":"10.1007\/s12975-016-0485-3","volume":"8","author":"E Atangana","year":"2017","unstructured":"Atangana E, Schneider UC, Blecharz K et al (2017) Intravascular inflammation triggers intracerebral activated microglia and contributes tosecondary brain injury after experimental subarachnoid hemorrhage (eSAH). 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