GSPE is superior to NAC in the prevention of contrast-induced nephropathy: Might this superiority be related to caspase 1 and calpain 1?

Ulusoy, Şükrü; Özkan, Gülsüm; Munğan, Sevdegül; Örem, Asım; Yuluğ, Esin; Alkanat, Mehmet; Yucesan, Fulya Balaban

doi:10.1016/j.lfs.2014.03.030

Cited by 19 publications

(16 citation statements)

References 33 publications

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“…34 Moreover, Ulusoy et al showed that the level of caspase 1 reduced in diabetes mellitus. 35 In line with the studies, the levels of caspase 1 and IL-1a, and IL-1b were determined to be higher in the diabetic group.…”

Section: Discussionsupporting

confidence: 70%

The effects of grape seed on apoptosis-related gene expression and oxidative stress in streptozotocin-induced diabetic rats

et al. 2015

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Background: Diabetic nephropathy is the most common cause of end-stage renal disease. Emerging evidences indicate that many mechanistic pathways including apoptosis play an important role in the pathogenesis and progression of macrovascular and microvascular complications of diabetes mellitus. The aim of the present study is to show the effects of grape seed extract (GSE) on oxidative stress and apoptosis in the kidney of streptozotocin-induced diabetic rats.

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Section: Discussionsupporting

confidence: 70%

The effects of grape seed on apoptosis-related gene expression and oxidative stress in streptozotocin-induced diabetic rats

et al. 2015

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“…45,46 A rise in NO can lead to apoptotic or necrotic injury in tubular epithelial cells. 35,47 While research suggests that a decrease in NO production is involved in the pathogenesis of CIN, clinical studies have not supported this finding. 34,47 Sphingolipids are novel second messengers mediating a variety of cellular responses, including cell proliferation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…35,47 While research suggests that a decrease in NO production is involved in the pathogenesis of CIN, clinical studies have not supported this finding. 34,47 Sphingolipids are novel second messengers mediating a variety of cellular responses, including cell proliferation and apoptosis. 23 Previous studies have shown that high concentrations of SPC induce apoptosis via the mitochondrial pathway.…”

Section: Discussionmentioning

confidence: 99%

Antioxidant and renoprotective effects of sphingosylphosphorylcholine on contrast-induced nephropathy in rats

Aksu

Unlu

et al. 2016

Renal Failure

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Contrast induced nephropathy (CIN) is a major cause of morbidity, and increased costs as well as an increased risk of death. This study was evaluated effects of exogenous sphingosylphosphorylcholine (SPC) administration on CIN in rats. Eight animals were included in each of the following eight groups: control, control phosphate-buffered solution (PBS), control SPC 2, control SPC 10, CIN, CIN PBS, CIN SPC 2 and CIN SPC 10. The induced nephropathy was created by injected with 4 g iodine/kg body weight. SPC was administered 3 d at a daily two different doses of 2 μm/mL and 10 μm/mL intraperitoneally. The severity of renal injury score was determined by the histological and immunohistochemical changes in the kidney. Malondialdehyde (MDA), nitric oxide (NO) and superoxide dismutase (SOD) were determined to evaluate the oxidative status in the renal tissue. Treatment with 2 and 10 μM SPC inhibited the increase in renal MDA, NO levels significantly and also attenuated the depletion of SOD in the renal injuryCIN. These data were supported by histopathological findings. The inducible nitric oxide synthase positive cells and apoptotic cells in the renal tissue were observed to be reduced with the 2 and 10 μM SPC treatment. These findings suggested that 2 and 10 μM doses can attenuate renal damage in contrast nephropathy by prevention of oxidative stress and apoptosis. The low and high dose SPC may be a promising new therapeutic agent for CIN.

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“…In addition to antioxidant, GSPE has antiviral, antibacterial, anti-inflammatory, and anti-apoptotic effects [15, 16]. Remarkably, GSPE also has unique properties that prevent kidney injury induced by colistin [17], cisplatin [18], and cyclosporine A [19].…”

Section: Introductionmentioning

confidence: 99%

GSPE reduces lead-induced oxidative stress by activating the Nrf2 pathway and suppressing miR153 and GSK-3β in rat kidney

et al. 2017

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Lead (Pb) is a global environmental health hazard that leads to nephrotoxicity. However, the effective treatment of Pb-induced nephrotoxicity remains elusive. Grape seed procyanidin extract (GSPE) has beneficial properties for multiple biological functions. Therefore, the present study investigated whether GSPE reduced Pb-induced nephrotoxicity as well as the protective mechanism of GSPE in a well-established 35-day Pb induced nephrotoxicity rat model. The results showed that GSPE normalized Pb-induced oxidative stress, histological damage, inflammatory, apoptosis, and changes of miR153 and glycogen synthase kinase 3β (GSK-3β) levels in rat kidney. Moreover, GSPE enhanced the induction of phase II detoxifying enzymes (heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1) by increasing nuclear factor-erythroid-2-related factor 2 (Nrf2) expression. This study identifies for the first time that Pb-induced oxidative stress in rat kidney is attenuated by GSPE treatment via activating Nrf2 signaling pathway and suppressing miR153 and GSK-3β. Nrf2 signaling provides a new therapeutic target for renal injury induced by Pb, and GSPE could be a potential natural agent to protect against Pb-induced nephrotoxicity.

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GSPE is superior to NAC in the prevention of contrast-induced nephropathy: Might this superiority be related to caspase 1 and calpain 1?

Cited by 19 publications

References 33 publications

The effects of grape seed on apoptosis-related gene expression and oxidative stress in streptozotocin-induced diabetic rats

The effects of grape seed on apoptosis-related gene expression and oxidative stress in streptozotocin-induced diabetic rats

Antioxidant and renoprotective effects of sphingosylphosphorylcholine on contrast-induced nephropathy in rats

GSPE reduces lead-induced oxidative stress by activating the Nrf2 pathway and suppressing miR153 and GSK-3β in rat kidney

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