{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T04:30:50Z","timestamp":1764131450951,"version":"3.41.0"},"reference-count":38,"publisher":"Canadian Science Publishing","issue":"8","license":[{"start":{"date-parts":[[2016,8,1]],"date-time":"2016-08-01T00:00:00Z","timestamp":1470009600000},"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":[[2016,8]]},"abstract":"<jats:p> The present study investigated the possible renoprotective effect of direct renin inhibitor (aliskiren) on renal dysfunctions, as well as its underlying mechanisms in rat model of adenine-induced tubulointerstitial nephropathy. Forty male Sprague-Dawley rats were randomized into 4 groups; normal group, aliskiren group (normal rats received 10 mg\/kg aliskiren), adenine group (animals received high-adenine diet for 4 weeks and saline for 12 weeks), and adenine + aliskiren group (animals received adenine for 4 weeks and aliskiren 10 mg\/kg for 12 weeks). It was found that adenine caused significant decrease in body mass, Hb, HR, serum Ca<jats:sup>2+<\/jats:sup>, eNOS and nrf2 expression, GSH, and catalase in kidney tissues with significant increase in arterial blood pressure (ABP), serum creatinine, BUN, plasma renin activity (PRA), K<jats:sup>+<\/jats:sup> and P, urinary albumin excretion (UAE), caspase-3, and MDA (lipid peroxidation marker) in kidney tissues compared to normal group (p &lt; 0.05). Administration of aliskiren caused significant improvement in all studied parameters compared to adenine group (p &lt; 0.05). We concluded that aliskiren has renoprotective effect against adenine-induced nephropathy. This might be due to inhibition of PRA, attenuation of oxidative stress, activation of Nrf2 and eNOS genes, and suppression of caspase-3. <\/jats:p>","DOI":"10.1139\/cjpp-2015-0364","type":"journal-article","created":{"date-parts":[[2016,2,12]],"date-time":"2016-02-12T22:35:23Z","timestamp":1455316523000},"page":"829-837","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Renoprotective effects of aliskiren on adenine-induced tubulointerstitial nephropathy: possible underlying mechanisms"],"prefix":"10.1139","volume":"94","author":[{"given":"Abdelaziz M.","family":"Hussein","sequence":"first","affiliation":[{"name":"Medical Physiology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hala Abdel","family":"Malek","sequence":"additional","affiliation":[{"name":"Clinical Pharmacology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mohamed-Ahdy","family":"Saad","sequence":"additional","affiliation":[{"name":"Clinical Pharmacology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.1177\/1470320314530178"},{"key":"refg2\/ref2","doi-asserted-by":"publisher","DOI":"10.1016\/j.fct.2013.12.038"},{"key":"refg3\/ref3","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0125285"},{"key":"refg4\/ref4","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gft022"},{"key":"refg5\/ref5","doi-asserted-by":"publisher","DOI":"10.1159\/000072913"},{"key":"refg6\/ref6","doi-asserted-by":"publisher","DOI":"10.1177\/1470320312474853"},{"key":"refg7\/ref7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.4.510"},{"key":"refg8\/ref8","doi-asserted-by":"publisher","DOI":"10.1002\/path.1289"},{"issue":"1","key":"refg9\/ref9","first-page":"44","volume":"23","author":"Fisher N.D.","year":"1994","journal-title":"Role of angiotensinII in humans. 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