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However, it is unclear, whether changes in<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 expression affect the endothelium<jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content>and what the underlying mechanism is. In the present study, we aimed to address this issue.<jats:styled-content style=\"fixed-case\">HG<\/jats:styled-content>\u2010treated human umbilical vascular endothelial cells (<jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>) were transfected by either<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3\u2010overexpressing (Ad\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3) or<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3\u2010sh<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010containing (Ad\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3\u2010sh<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>) adenoviral vectors. Likewise, the rats fed by high\u2010fat diet (<jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>) were infected by intravenous administration of Ad\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 or Ad\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3\u2010sh<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>. The levels of nitric oxide (<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>), endothelin\u20101 (<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101) and cytokines (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u03b1,<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106,<jats:styled-content style=\"fixed-case\">sICAM<\/jats:styled-content>\u20101 and<jats:styled-content style=\"fixed-case\">sVCAM<\/jats:styled-content>\u20101) and the expression levels of<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3,<jats:styled-content style=\"fixed-case\">eNOS<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\">AKT<\/jats:styled-content>, p\u2010<jats:styled-content style=\"fixed-case\">AKT<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\">IKK<\/jats:styled-content>\u03b1\/\u03b2 and p\u2010<jats:styled-content style=\"fixed-case\">IKK<\/jats:styled-content>\u03b1\/\u03b2 and I\u03baB\u03b1 were examined; and the interaction between<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 and<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u03baB\u2010P65 as well as vascular function were evaluated. Our present results showed that overexpression of<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 notably increased the levels of<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\">eNOS<\/jats:styled-content>, p\u2010<jats:styled-content style=\"fixed-case\">AKT<\/jats:styled-content>and I\u03baB\u03b1 as well as the interaction of<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 and<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u03baB\u2010P65, and decreased the levels of<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101, p\u2010<jats:styled-content style=\"fixed-case\">IKK<\/jats:styled-content>\u03b1\/\u03b2,<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u03b1,<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106,<jats:styled-content style=\"fixed-case\">sICAM<\/jats:styled-content>\u20101 and<jats:styled-content style=\"fixed-case\">sVCAM<\/jats:styled-content>\u20101. In contrast, down\u2010expression of<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 displayed the opposite effects. The results demonstrate that the overexpression of<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 improves while the down\u2010expression worsens the endothelium<jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content>via a<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3\u2010mediated<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u03baB trans\u2010repression dependent manner. The findings suggest<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 is a potential therapeutic target for diabetic vascular complications.<\/jats:p>","DOI":"10.1111\/jcmm.13913","type":"journal-article","created":{"date-parts":[[2018,11,6]],"date-time":"2018-11-06T06:25:44Z","timestamp":1541485544000},"page":"216-226","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Trans\u2010repression of<scp>NF<\/scp>\u03baB pathway mediated by<scp>PPAR<\/scp>\u03b3 improves vascular endothelium insulin resistance"],"prefix":"10.1111","volume":"23","author":[{"given":"Ying","family":"Kong","sequence":"first","affiliation":[{"name":"Key Provincial Laboratory of Basic Pharmacology Nanchang University Nanchang Jiangxi China"},{"name":"Department of Pharmacology School of Pharmacy Nanchang University Nanchang Jiangxi 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