Pyrrolidine dithiocarbamate attenuates the development of monocrotaline-induced pulmonary arterial hypertension

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dc.authoridsilan, coskun/0000-0002-8352-6571
dc.contributor.authorYavuz, Taner
dc.contributor.authorUzun, Ozge
dc.contributor.authorMacit, Asli
dc.contributor.authorComunoglu, Cem
dc.contributor.authorYavuz, Ozlem
dc.contributor.authorSilan, Coskun
dc.contributor.authorYuksel, Hatice
dc.date.accessioned2025-01-27T20:47:27Z
dc.date.available2025-01-27T20:47:27Z
dc.date.issued2013
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractWe aimed to demonstrate the potential protective effects of pyrrolidine dithiocarbamate (PDTC) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). Adult male rats were randomly assigned to 4 groups: control group, MCT-treated rats only, MCT-injected rats treated with PDTC, and PDTC-treated rats only. Blood and tissue samples were collected after the sacrifice. Levels of malondialdehyde (MDA) were measured by using the thiobarbituric acid method. Total antioxidant status (TAS) was determined using a commercially available ImAnOx kit. A histopathological evaluation was accomplished by scoring the degree of severity. Endothelial damage of the main pulmonary artery was evaluated by immunohistochemical labeling of endothelial cells using anti-rat endothelial cell antigen 1 (RECA-1) antibody. MCT-induced right ventricular hypertrophy (RVH) was reduced significantly in the MCT + PDTC-treated group. MDA levels were significantly lowered in the MCT + PDTC-treated group. TAS was significantly higher in the MCT + PDTC-treated group when compared with the rats with PAH. Histopathological examination demonstrated that PDTC treatment reduced the development of inflammation, hemorrhage and congestion, and collagen deposition. In conclusion, PDTC attenuated PAH and protected pulmonary endothelium in rats administered MCT. These findings suggest that PDTC treatment may provide a new effective therapeutic approach in the treatment of PAH. (C) 2013 Elsevier GmbH. All rights reserved.
dc.identifier.doi10.1016/j.prp.2013.03.002
dc.identifier.endpage308
dc.identifier.issn0344-0338
dc.identifier.issue5
dc.identifier.pmid23582365
dc.identifier.startpage302
dc.identifier.urihttps://doi.org/10.1016/j.prp.2013.03.002
dc.identifier.urihttps://hdl.handle.net/20.500.12428/24911
dc.identifier.volume209
dc.identifier.wosWOS:000321090000006
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Gmbh, Urban & Fischer Verlag
dc.relation.ispartofPathology Research and Practice
dc.relation.publicationcategoryinfo:eu-repo/semantics/openAccess
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20250125
dc.subjectImmunohistochemistry
dc.subjectMonocrotaline
dc.subjectNF-kappa B
dc.subjectPulmonary arterial hypertension
dc.subjectPyrrolidine dithiocarbamate
dc.titlePyrrolidine dithiocarbamate attenuates the development of monocrotaline-induced pulmonary arterial hypertension
dc.typeArticle

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