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Cardiovascular Changes Related to Metabolic Syndrome: Evidence in Obese Zucker Rats

Metabolic syndrome (MetS) is a predictor of cardiovascular diseases, commonly
associated with oxidative stress and inflammation. However, the pathogenic mechanisms
are not yet fully elucidated. The aim of the study is to evaluate the oxidative status and
inflammation in the heart of obese Zucker rats (OZRs) and lean Zucker rats (LZRs) at different
ages. Morphological and morphometric analyses were performed in the heart. To study the
oxidative status, the malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), protein oxidation,
and antioxidant enzymes were measured in plasma and heart. To elucidate the inflammatory
markers involved, immunohistochemistry and Western blot were performed for cellular adhesion
molecules and proinflammatory cytokines. OZRs were characterized by hypertension, hyperlipidemia,
hyperglycemia, and insulin resistance. The obesity increased MDA and decreased the activities
of superoxide dismutase (SOD) in plasma as well as in the heart, associated with cardiomyocytes
hypertrophy. OxyBlot in plasma and in heart showed an increase of oxidativestate proteins in OZRs.
Vascular cell adhesion molecule-1, interleukin-6, and tumor necrosis factor-α expressions in OZRs
were higher than those of LZRs. However, these processes did not induce apoptosis or necrosis of
cardiomyocytes. Thus, MetS induces the lipid peroxidation and decreased antioxidant defense that
leads to heart tissue changes and coronary inflammation

Identiferoai:union.ndltd.org:DRESDEN/oai:qucosa:de:qucosa:88967
Date11 January 2024
CreatorsMartinelli, Ilenia, Tomassoni, Daniele, Moruzzi, Michele, Roy, Proshanta, Cifani, Carlo, Amenta, Francesco, Tayebati, Seyed Khosrow
PublisherMDPI
Source SetsHochschulschriftenserver (HSSS) der SLUB Dresden
LanguageEnglish
Detected LanguageEnglish
Typeinfo:eu-repo/semantics/publishedVersion, doc-type:article, info:eu-repo/semantics/article, doc-type:Text
Rightsinfo:eu-repo/semantics/openAccess
Relation2035, 10.3390/ijms21062035

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