{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,3]],"date-time":"2025-07-03T04:08:22Z","timestamp":1751515702422,"version":"3.41.0"},"reference-count":71,"publisher":"Canadian Science Publishing","issue":"10","license":[{"start":{"date-parts":[[2020,10,1]],"date-time":"2020-10-01T00:00:00Z","timestamp":1601510400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:p> Glucocorticoid therapy has been associated with adverse cardiometabolic effects during pregnancy. Inflammation-mediated cardiac dysfunction, an independent risk factor for morbidity and mortality, has been linked to defective glucose-6-phosphate dehydrogenase (G6PD) dependent antioxidant defenses and increased endoglin expression. We therefore sought to investigate the effects of dexamethasone (DEX) on cardiac endoglin and G6PD-dependent antioxidant defense. Twenty-four rats were randomly assigned to nonpregnant (PRE(\u2013)), DEX-exposed nonpregnant (PRE(\u2013) + DEX), pregnant (PRE(+)), and DEX-exposed pregnant (PRE(+) + DEX) rats, respectively (n = 6 per group). PRE(\u2013) and PRE(+) rats received vehicle (per oral (po)), while PRE(\u2013) + DEX and PRE(+) + DEX groups were administered DEX (0.2 mg\/kg po) between gestational days 14 and 19, respectively. Results showed that DEX caused increased cardiac pro-inflammatory markers (adenosine deaminase (ADA) activity, endoglin, vascular cell adhesion molecule-1 (VCAM-1), tissue injury markers (LDH, GGT, AST, ALT, and ALP), metabolic disturbances (elevated fasting plasma glucose, free fatty acid (FFA), lactate, cardiac FFA, and lactate) and depressed G6PD-dependent antioxidant defenses (G6PD activity, reduced glutathione\/oxidized glutathione ratio, and nitric oxide) in pregnant and nonpregnant rats. The present study demonstrates that DEX led to increased cardiac endoglin and VCAM-1 that is accompanied by defective G6PD-dependent antioxidant defenses but not cardiac lipid accumulation in both pregnant and nonpregnant rats. <\/jats:p>","DOI":"10.1139\/cjpp-2018-0351","type":"journal-article","created":{"date-parts":[[2020,4,7]],"date-time":"2020-04-07T22:15:46Z","timestamp":1586297746000},"page":"667-677","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Dexamethasone causes defective glucose-6-phosphate dehydrogenase dependent antioxidant barrier through endoglin in pregnant and nonpregnant rats"],"prefix":"10.1139","volume":"98","author":[{"given":"Olufunto O.","family":"Badmus","sequence":"first","affiliation":[{"name":"HOPE Cardiometabolic Research Team and Department of Physiology, College of Health Sciences, University of Ilorin, Ilorin, Nigeria."},{"name":"Department of Public Health, Kwara State University, Malete, Nigeria."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lawrence A.","family":"Olatunji","sequence":"additional","affiliation":[{"name":"HOPE Cardiometabolic Research Team and Department of Physiology, College of Health Sciences, University of Ilorin, Ilorin, Nigeria."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijcard.2004.05.009"},{"key":"refg2\/ref2","doi-asserted-by":"publisher","unstructured":"Assad, R.S., Atik, F.A., Oliveira, F.S., Fonseca-Alaniz, M.H., Abduch, M.C., Silva, G.J. et al. 2011. 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