{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T20:06:10Z","timestamp":1786133170562,"version":"build-2736575974"},"reference-count":0,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,8]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract.<\/jats:title>\n                    <jats:p>\n                      Nitric oxide (NO) regulates inflammatory responses partly by cell-specific inhibition of the transcription factor nuclear factor \u03baB (NF-\u03baB). This study investigated the effect of continuous oral administration of an NO donor (molsidomine [Mol]), NO precursor (L-arginine [L-arg]), or selective inhibitors of inducible NO synthase (iNOS; aminoguanidine [AG], L-\n                      <jats:italic toggle=\"yes\">N<\/jats:italic>\n                      <jats:sup>6<\/jats:sup>\n                      -(1-iminoethyl)lysine [L-NIL]) on the progression of tubulointerstitial inflammation and NF-\u03baB activation in a non-immune model of chronic glomerular disease (Adriamycin nephropathy [AN]), from day 8 until day 30 after disease induction. On day 30, rats with AN had heavy proteinuria, reduced creatinine clearance, and tubulointerstitial disease. Treatment with both AG and L-NIL exacerbated the progression of AN as evidenced by (\n                      <jats:italic toggle=\"yes\">1<\/jats:italic>\n                      ) increased renal cortical malondialdehyde; (\n                      <jats:italic toggle=\"yes\">2<\/jats:italic>\n                      ) reduced creatinine clearance; and (\n                      <jats:italic toggle=\"yes\">3<\/jats:italic>\n                      ) increased tubular atrophy, interstitial volume, and monocyte infiltration. Unexpectedly, Mol also increased renal malondialdehyde and worsened tubular injury, whereas L-arg had no effect. The increase in renal cortical NF-\u03baB activation in AN was not altered by AG, L-NIL, or Mol, but the mRNA expression of monocyte chemoattractant protein-1, interleukin-10, and osteopontin were elevated in these groups. Nitrite release from kidney slices reduced in AN. Treatment with Mol restored renal nitrite release to normal, whereas neither L-arg nor the NOS inhibitors had an effect. It is concluded that endogenous iNOS-derived NO has a protective role against tubulointerstitial injury and cytokine production in AN. However, the pro-oxidant activity of NO donors may limit their potential benefit in proteinuric renal disease.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.v1281696","type":"journal-article","created":{"date-parts":[[2021,4,26]],"date-time":"2021-04-26T20:57:00Z","timestamp":1619470620000},"page":"1696-1705","source":"Crossref","is-referenced-by-count":22,"title":["Pharmacologic Modulators of Nitric Oxide Exacerbate Tubulointerstitial Inflammation in Proteinuric Rats"],"prefix":"10.1681","volume":"12","author":[{"given":"GOPALA K.","family":"RANGAN","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YIPING","family":"WANG","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"DAVID C. H.","family":"HARRIS","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","container-title":["Journal of the American Society of Nephrology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ovid.com\/00001751-200108000-00013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T19:29:46Z","timestamp":1786130986000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ovid.com\/00001751-200108000-00013"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2001,8]]},"references-count":0,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2001]]}},"URL":"https:\/\/doi.org\/10.1681\/asn.v1281696","relation":{},"ISSN":["1046-6673"],"issn-type":[{"value":"1046-6673","type":"print"}],"subject":[],"published":{"date-parts":[[2001,8]]}}}