| http://purl.uniprot.org/citations/36647295 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/36647295 | http://www.w3.org/2000/01/rdf-schema#comment | "Sepsis-induced myocardial injury is a consequence of septicemia and is one of the major causes of death in intensive care units. A serum glycoprotein called fetuin-A is secreted largely by the liver, tongue, placenta, and adipose tissue. Fetuin-A has a variety of biological and pharmacological properties. The anti-inflammatory and antioxidant glycoprotein fetuin-A has shown its efficacy in a number of inflammatory disorders including sepsis. However, its protective role against sepsis-induced myocardial injury remains elusive. The purpose of this work is to explore the role of fetuin-A in mouse models of myocardial injury brought on by cecal ligation and puncture (CLP). CLP significantly induced the myocardial injury assessed in terms of elevated myocardial markers (serum CK-MB, cTnI levels), inflammatory markers (IL-6, TNF-α) in the serum, and oxidative stress markers (increased MDA levels and decreased reduced glutathione) in heart tissue homogenate following 24 h of ligation and puncture. Further, hematoxylin and eosin (H&E) staining showed considerable histological alterations in the myocardial tissue of sepsis-developed mice. Interestingly, fetuin-A pretreatment (50 and 100 mg/kg) for 4 days before the CLP procedure significantly improved the myocardial injury and was evaluated in perspective of a reduction in the CK-MB, cTnI levels, IL-6, and TNF-α in sepsis-developed animals. Fetuin-A pretreatment significantly attenuated the oxidative stress and improved the myocardial morphology in a dose-dependent manner. The present study provides preliminary evidence that fetuin-A exerts protection against sepsis-induced cardiac dysfunction in vivo via suppression of inflammation and oxidative damage."xsd:string |
| http://purl.uniprot.org/citations/36647295 | http://purl.org/dc/terms/identifier | "doi:10.1111/fcp.12870"xsd:string |
| http://purl.uniprot.org/citations/36647295 | http://purl.uniprot.org/core/author | "Bali A."xsd:string |
| http://purl.uniprot.org/citations/36647295 | http://purl.uniprot.org/core/author | "Navik U."xsd:string |
| http://purl.uniprot.org/citations/36647295 | http://purl.uniprot.org/core/author | "Hanifa M."xsd:string |
| http://purl.uniprot.org/citations/36647295 | http://purl.uniprot.org/core/author | "Sidheeque Hassan V."xsd:string |
| http://purl.uniprot.org/citations/36647295 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
| http://purl.uniprot.org/citations/36647295 | http://purl.uniprot.org/core/name | "Fundam Clin Pharmacol"xsd:string |
| http://purl.uniprot.org/citations/36647295 | http://purl.uniprot.org/core/pages | "607-617"xsd:string |
| http://purl.uniprot.org/citations/36647295 | http://purl.uniprot.org/core/title | "Exogenous fetuin-A protects against sepsis-induced myocardial injury by inhibiting oxidative stress and inflammation in mice."xsd:string |
| http://purl.uniprot.org/citations/36647295 | http://purl.uniprot.org/core/volume | "37"xsd:string |
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