Abstract:
BACKGROUND/AIMS:Chronic renal allograft dysfunction (CRAD) is a leading cause of long-term renal allograft loss. Oxidative stress may account for the nonspecific interstitial fibrosis and tubular atrophy that occur in CRAD. An antioxidant intervention via Nrf2 signaling pathway activation might be a promising therapy for some kidney diseases. The present paper investigates whether there is an association between oxidative stress alleviation via sulforaphane-induced Nrf2-HO-1/NQO-1 signaling pathway activation and CRAD improvement. METHODS:F344 rat kidneys were orthotopically transplanted into Lewis rat recipients to establish CRAD models. Sulforaphane was administered at 1.5 mg/kg intraperitoneally once daily. Renal function and 24-hour urinary protein were monitored for variations for 24 weeks after transplantation. After 24 weeks, renal histopathology was evaluated according to the Banff criteria after hematoxylin and eosin, Masson's trichrome and periodic acid-Schiff stainings. Additionally, intrarenal oxidative stress was assessed by the indicators malondialdehyde, 8-isoprostane, oxidized-low density lipoprotein and 8-hydroxy-2'-deoxyguanosine, as well as the activity levels of the antioxidant enzymes total superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and γ-glutamylcysteine synthetase. Nrf2, HO-1 and NQO-1 expression levels were determined via immunohistochemical and Western blot analyses. RESULTS:The sulforaphane-induced Nrf2-HO-1/NQO-1 signaling pathway activation, as demonstrated by immunohistochemical and Western blot analyses, delayed the progression of serum creatinine and blood urea nitrogen, particularly lowering the 24-hour urinary protein levels of CRAD. The semi-quantified histopathological changes were also alleviated. Evidence of oxidative stress alleviation, as indicated by a concurrent decrease in the indicators and sustained levels of antioxidant enzymes activity, was found in the renal allografts after sulforaphane intervention. CONCLUSION:Oxidative stress alleviation caused by continuous sulforaphane-induced Nrf2-HO-1/NQO-1 signaling pathway activation is associated with functional and morphological improvements of CRAD.
journal_name
Kidney Blood Press Resjournal_title
Kidney & blood pressure researchauthors
Lv D,Zhou Q,Xia Y,You X,Zhao Z,Li Y,Zou Hdoi
10.1159/000487501subject
Has Abstractpub_date
2018-01-01 00:00:00pages
191-205issue
1eissn
1420-4096issn
1423-0143pii
000487501journal_volume
43pub_type
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journal_title:Kidney & blood pressure research
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journal_title:Kidney & blood pressure research
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doi:10.1159/000025950
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journal_title:Kidney & blood pressure research
pub_type: 杂志文章,评审
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更新日期:2014-01-01 00:00:00
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pub_type: 杂志文章,随机对照试验
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doi:10.1159/000508372
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journal_title:Kidney & blood pressure research
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pub_type: 临床试验,杂志文章,随机对照试验
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journal_title:Kidney & blood pressure research
pub_type: 杂志文章,评审
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更新日期:2004-01-01 00:00:00
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journal_title:Kidney & blood pressure research
pub_type: 临床试验,杂志文章
doi:10.1159/000066348
更新日期:2002-01-01 00:00:00
abstract::Inhibitors of angiotensin-converting enzyme (ACE) or beta isoforms of protein kinase C (PKC) are nephroprotective in diabetes mellitus. We investigated the influence of streptozotocin (STZ)-induced diabetes mellitus and of treatment with the ACE inhibitor lisinopril (4 mg/kg p.o. twice daily for 4 weeks) on the expres...
journal_title:Kidney & blood pressure research
pub_type: 杂志文章
doi:10.1159/000066789
更新日期:2002-01-01 00:00:00
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更新日期:2010-01-01 00:00:00
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journal_title:Kidney & blood pressure research
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更新日期:2014-01-01 00:00:00
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doi:10.1159/000350064
更新日期:2013-01-01 00:00:00
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更新日期:2013-01-01 00:00:00