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Pharmacological inhibition of nuclear factor <jats:italic>kappa<\/jats:italic>B (<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u043aB) with pyrrolidine dithiocarbamate (<jats:styled-content style=\"fixed-case\">PDTC<\/jats:styled-content>) can prevent <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content> up\u2010regulation. We suggested that treatment with <jats:styled-content style=\"fixed-case\">PDTC<\/jats:styled-content> could prevent 2\u2010kidney, 1\u2010clip (2K1C) hypertension\u2010induced left ventricular remodelling. Sham\u2010operated controls or 2K1C rats with hypertension received either vehicle or <jats:styled-content style=\"fixed-case\">PDTC<\/jats:styled-content> (100\u00a0mg\/kg\/day) by gavage for 8\u00a0weeks. Systolic blood pressure was monitored every week. Histological assessment of left ventricles was carried out with haematoxylin\/eosin sections, and fibrosis was quantified in picrosirius red\u2010stained sections. Oxidative stress was evaluated in heart samples with the dihydroethidium probe. Cardiac <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content> activity was determined by <jats:italic>in situ<\/jats:italic> zymography, and cardiac <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\u20102 was assessed by immunofluorescence. 2K1C surgery significantly increased systolic blood pressure in the 2K1C\u00a0vehicle. <jats:styled-content style=\"fixed-case\">PDTC<\/jats:styled-content> exerted antihypertensive effects after 2\u00a0weeks of treatment. Histology revealed increased left ventricular and septum wall thickness associated with augmented myocyte diameter in hypertensive rats, which were reversed by treatment with <jats:styled-content style=\"fixed-case\">PDTC<\/jats:styled-content>. Hypertensive rats developed pronounced cardiac fibrosis with increased interstitial collagen area, increased cardiac reactive oxygen species levels, gelatinase activity and <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\u20102 expression. <jats:styled-content style=\"fixed-case\">PDTC<\/jats:styled-content> treatment decreased these alterations. These findings show that <jats:styled-content style=\"fixed-case\">PDTC<\/jats:styled-content> modulates myocardial <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\u20102 expression and ameliorates cardiac remodelling in renovascular hypertension. These results suggest that interfering with <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content> expression at transcriptional level may be an interesting strategy in the therapy of organ damage associated with hypertension.<\/jats:p>","DOI":"10.1111\/bcpt.12400","type":"journal-article","created":{"date-parts":[[2015,3,29]],"date-time":"2015-03-29T07:04:30Z","timestamp":1427612670000},"page":"234-241","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["The Nuclear Factor <i>kappa<\/i>B Inhibitor Pyrrolidine Dithiocarbamate Prevents Cardiac Remodelling and Matrix Metalloproteinase\u20102 Up\u2010Regulation in Renovascular Hypertension"],"prefix":"10.1111","volume":"117","author":[{"given":"Stefany B. 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