The presence of oxidized low‐density lipoprotein and inducible nitric oxide synthase expression in renal damage after intestinal ischemia reperfusion

Yurdakan, Gamze; Tekin, İshak Özel; Comert, Mustafa; Açıkgöz, Şerefden; Sipahi, Emine Yılmaz

doi:10.1016/j.kjms.2011.06.030

Cited by 15 publications

(16 citation statements)

References 38 publications

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“…MDA, which is an end-product derived from the breakdown of polyunsaturated fatty acids and related esters, provides a convenient index of lipid peroxidation [28]. 8-isoprostane is also a reliable and specific in vivo marker of oxidative stress produced by free radical peroxidation of arachidonic acid [29], while ox-LDL can further reflect early lipid peroxidation [30]. 8-OHdG is a biomarker of oxidative damage to DNA and is, therefore, another well-accepted index of oxidative stress [31-32].…”

Section: Discussionmentioning

confidence: 99%

The Association Between Oxidative Stress Alleviation via Sulforaphane-Induced Nrf2-HO-1/NQO-1 Signaling Pathway Activation and Chronic Renal Allograft Dysfunction Improvement

Zhou

Xia

et al. 2018

Kidney Blood Press Res

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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.

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Section: Discussionmentioning

confidence: 99%

The Association Between Oxidative Stress Alleviation via Sulforaphane-Induced Nrf2-HO-1/NQO-1 Signaling Pathway Activation and Chronic Renal Allograft Dysfunction Improvement

Zhou

Xia

et al. 2018

Kidney Blood Press Res

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“…[3], [4], [15] As pre-conditioning plays a role through a number of signaling pathways, the renal-protective effects in IIR-treated mice might be enhanced by activation of the Nrf2/ARE pathway. [16] In the present study, Nrf2 expression was significantly higher in the IIR group than that observed in the Sham group, which suggests the activation of the Nrf2/ARE pathway in the kidneys following IIR treatment.…”

Section: Discussionmentioning

confidence: 99%

“…[2] Recent studies have shown that IIR causes significant oxidative injury in rat renal parenchyma, consisting of severe alterations observed at the level of subcellular renal structures, and is associated with significant failure of kidney function. [3], [4] …”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Ginsenoside Rb1 against Intestinal Ischemia-Reperfusion Induced Acute Renal Injury in Mice

et al. 2013

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Ginsenoside Rb1 (RB1), the most clinically effective constituent of ginseng, possesses a variety of biological activities. The objectives of this study were to investigate the protective effects of RB1 and its underlying mechanism on renal injury induced by intestinal ischemia-reperfusion (IIR) in mice. RB1 was administered prior to inducing IIR achieved by occluding the superior mesenteric artery for 45 min followed by 120 min of reperfusion. All-trans-retinoic acid (ATRA) was used as an inhibitor of NF-E2-related factor-2 (Nrf2) signaling. Adult male C57BL/6J mice were randomly divided into six groups: (1) sham group, (2) IIR group, (3) RB1 group, (4) sham + ATRA group, (5) IIR + ATRA group, and (6) RB1 + ATRA group. Intestinal histology and pathological injury score were observed. Intestinal mucosal injury was also evaluated by measuring serum diamine oxidase (DAO). Renal injury induced by IIR was characterized by increased levels of histological severity score, blood urea nitrogen (BUN), serum creatinine (Scr) and neutrophil gelatinase-associated lipocalin (NGAL), which was accompanied with elevated renal TUNEL-positive cells and the Bcl-2/Bax expression ratio. RB1 significantly reduced renal injury and apoptosis as compared with IIR group, which was reversed by ATRA treatment. Immunohistochemistry and Western blot analysis demonstrated that RB1 significantly upregulated the protein expression of heme oxygenase-1 (HO-1) and Nrf2, which were attenuated by ATRA treatment. Taken together, these results suggest that the protective effects of RB1 pretreatment against renal injury induced by IIR are associated with activation of the Nrf2/ anti-oxidant response element (ARE) pathway.

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“…Myocardial I/R is known to upregulate lectin-like oxLDL receptors which have been associated with apoptosis, necrosis, and left ventricular functional deterioration [28], while activation of the lectin-like oxidized low-density lipoprotein receptor-1 pathway is involved in determining the extent of myocardial ischaemia-reperfusion injury [29]. Also, oxLDL may play a role in renal tissue damage after intestinal I/R [30]. Given the aforementioned significant evidence, as well as the fact that our animals were monitored for only 2 hours after reperfusion, further research is warranted to fully clarify the role of oxLDL after abdominal aortic clamping.…”

Section: Discussionmentioning

confidence: 99%

The effects of n-acetylcysteine and desferoxamine on IL-6, TNF-a, and oxLDL after infrarenal aortic clamping

Katseni¹,

Chalkias

Kaparos³

et al. 2015

Hellenic J Surg

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Aim-Background: Treatment of abdominal aortic aneurysms remains a challenging task. We examined the effects of n-acetylcysteine and desferoxamine on interleukin-6, tumour necrosis factor-a, and oxidized low density lipoprotein after infrarenal aortic clamping.Methods: Fifteen piglets were assigned to three groups. The control group (Group C) received saline as placebo (10-mL dilution, bolus), whereas the Group of n-acetylcysteine (Group NAC) received 150mg/kg IV n-acetylcysteine 30 min prior to aortic clamping and 50mg/kg/h after its release (reperfusion). The desferoxamine group (Group D) received IM 100mg/kg/d desferoxamine for 3 days prior to the experiment.Results: Interleukin-6 increased significantly one hour after aortic clamping, while administration of desferoxamine and n-acetylcysteine had no effect on its production. Tumour necrosis factor-a increased after aortic clamping and failed to normalise during the experiment in all groups. At 2 hours post-reperfusion, desferoxamine had a modest effect on tumour necrosis factor-a values, while in Group NAC, tumour necrosis factor-a had decreased by 50% at 10 min post-reperfusion. Oxidized low density lipoprotein in Group C did not increase significantly from baselines values. In Groups D and NAC, oxidized low density lipoprotein had increased at 10 min post-reperfusion, after which it progressively decreased until 2 hours post-reperfusion.Conclusions: Interleukin-6 and tumour necrosis factor-a increased significantly after aortic clamping. Administration of desferoxamine and n-acetylcysteine had no effect on interleukin-6, while administration of n-acetylcysteine reduced tumour necrosis factor-a by 50% at 10 min post-reperfusion. Although in Groups D and NAC oxidized low density lipoprotein increased post-reperfusion, it progressively decreased with time.

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The presence of oxidized low‐density lipoprotein and inducible nitric oxide synthase expression in renal damage after intestinal ischemia reperfusion

Cited by 15 publications

References 38 publications

The Association Between Oxidative Stress Alleviation via Sulforaphane-Induced Nrf2-HO-1/NQO-1 Signaling Pathway Activation and Chronic Renal Allograft Dysfunction Improvement

The Association Between Oxidative Stress Alleviation via Sulforaphane-Induced Nrf2-HO-1/NQO-1 Signaling Pathway Activation and Chronic Renal Allograft Dysfunction Improvement

Protective Effect of Ginsenoside Rb1 against Intestinal Ischemia-Reperfusion Induced Acute Renal Injury in Mice

The effects of n-acetylcysteine and desferoxamine on IL-6, TNF-a, and oxLDL after infrarenal aortic clamping

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