Nephroprotective potential of carnitine against glycerol and contrast-induced kidney injury in rats through modulation of oxidative stress, proinflammatory cytokines, and apoptosis

Kunak, Celalettin Semih; Uğan, Rüstem Anıl; Çadırcı, Elif; Karakuş, Emre; Polat, Beyzagül; Un, Harun; Halıcı, Zekai; Sarıtemur, Murat; Atmaca, Hasan; Karaman, Adem

doi:10.1259/bjr.20140724

Cited by 35 publications

(22 citation statements)

References 69 publications

(87 reference statements)

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“…Decreased SOD activity and GSH levels have previously been reported in CIN, and different treatment strategies have ameliorated oxidative stress. 23 , 26 In accordance with the results of our study, Saritemur et al. showed decreased SOD activity and GSH levels in GLY-aggravated CIN, and treatment with infliximab increased SOD activity and GSH levels.…”

Section: Discussionsupporting

confidence: 92%

“…Oxidative stress, the perturbation of the balance between pro-oxidants and antioxidants, may underline the pathology of CIN. 23 , 26 EGCG has antioxidant activity, which is attributed to the galloyl group at the 3 position and the o-trihydroxyl group in the B ring in its structure, and it protects cells from damage by reactive oxygen species (ROS). Thus, EGCG may have an antioxidant effect on oxidative stress-induced impaired renal function.…”

Section: Discussionmentioning

confidence: 99%

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A new update for radiocontrast-induced nephropathy aggravated with glycerol in rats: the protective potential of epigallocatechin-3-gallate

et al. 2017

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Contrast media (CM) is known to have nephrotoxic adverse effects. Epigallocatechin-3-gallate (EGCG) is the most abundant and active catechin in green tea, and has strong antioxidant and anti-inflammatory properties. This study investigated whether EGCG can reduce contrast-induced nephrotoxicity (CIN), alone or with glycerol (GLY)-induced renal damage, and to understand its mechanisms of protection against toxicity, using models of GLY and CIN in rats. The rats were separated into eight groups (n = 6 in each), as follows: Healthy, GLY, CM, GLY + CM, CM + EGCG 50 mg/kg (po), GLY + CM + EGCG 50 mg/kg (po), CM + EGCG 100 mg/kg (po), and GLY + CM + EGCG 100 mg/kg (po). Both doses of EGCG protected against CM-induced renal dysfunction, as measured by serum creatinine and blood urea nitrogen (BUN). In addition, EGCG treatment markedly improved CIN-induced oxidative stress, and resulted in a significant down-regulatory effect on tumor necrosis factor (TNF)-α and nuclear factor (NF)-κB mRNA expression. Moreover, histopathological analysis showed that EGCG also attenuated CM-induced kidney damage. Considering the potential clinical use of CM and the numerous health benefits of EGCG, this study showed the protective role of multi-dose EGCG treatment on CIN and GLY-aggravated CIN through different mechanisms.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

A new update for radiocontrast-induced nephropathy aggravated with glycerol in rats: the protective potential of epigallocatechin-3-gallate

et al. 2017

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“…All of the studies demonstrated the renoprotective effect by attenuating serum Cr and renal histological damage through their antioxidant activities (Table 4). Both inflammatory process and apoptosis were decreased following antioxidant treatments [35][36][37][38][42][43][44]. Active component of herbs; such as astragaloside, [45] curcumin, [46] grape seed proanthocyanidin, [47] lycopene, [48] magnolin (major active ingredient of herb Magnolia fargesii), [49] Phyllanthus emblica extract, [50] salidroside, [40] sesame oil, [51] and silymarin, [52] were investigated in CIN in rats (Table 4).…”

Section: Antioxidants As Interventions To Reduce Cinmentioning

confidence: 99%

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Kusirisin

Chattipakorn

2020

J Transl Med

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Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI) is an iatrogenic acute kidney injury observed after intravascular administration of contrast media for intravascular diagnostic procedures or therapeutic angiographic intervention. High risk patients including those with chronic kidney disease (CKD), diabetes mellitus with impaired renal function, congestive heart failure, intraarterial intervention, higher volume of contrast, volume depletion, old age, multiple myeloma, hypertension, and hyperuricemia had increased prevalence of CIN. Although CIN is reversible by itself, some patients suffer this condition without renal recovery leading to CKD or even end-stage renal disease which required long term renal replacement therapy. In addition, both CIN and CKD have been associated with increasing of mortality. Three pathophysiological mechanisms have been proposed including direct tubular toxicity, intrarenal vasoconstriction, and excessive production of reactive oxygen species (ROS), all of which lead to impaired renal function. Reports from basic and clinical studies showing potential preventive strategies for CIN pathophysiology including low- or iso-osmolar contrast media are summarized and discussed. In addition, reports on pharmacological interventions to reduce ROS and attenuate CIN are summarized, highlighting potential for use in clinical practice. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating CIN.

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“…L-carnitine is a naturally occurring amino acid derivative synthesized in the liver and kidney, it acts as a carrier for fatty acids acrossing the inner mitochondrial membrane, which is necessary for subsequent β-oxidation and ATP production [9]. The compound has been considered as a specific inhibitor of mitochondrial reactive oxygen species (ROS) [10], and the beneficial effects of which to protect kidney cells against oxidative stress, lipid peroxidation, proinflammatory cytokines, and apoptosis during acute and chronic kidney injury have been documented [11][12][13]. These pathogenetic factors have also been reported to play pivotal part in renal stone formation [14].…”

Section: Introductionmentioning

confidence: 99%

L-Carnitine Protects Renal Tubular Cells Against Calcium Oxalate Monohydrate Crystals Adhesion Through Preventing Cells From Dedifferentiation

Li¹,

Wu²,

Duan³

et al. 2016

Kidney Blood Press Res

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Background/Aims: The interactions between calcium oxalate monohydrate (COM) crystals and renal tubular epithelial cells are important for renal stone formation but still unclear. This study aimed to investigate changes of epithelial cell phenotype after COM attachment and whether L-carnitine could protect cells against subsequent COM crystals adhesion. Methods: Cultured MDCK cells were employed and E-cadherin and Vimentin were used as markers to estimate the differentiate state. AlexaFluor-488-tagged COM crystals were used in crystals adhesion experiment to distinguish from the previous COM attachment, and adhesive crystals were counted under fluorescence microscope, which were also dissolved and the calcium concentration was assessed by flame atomic absorption spectrophotometry. Results: Dedifferentiated MDCK cells induced by transforming growth factor β1 (TGF-β1) shown higher affinity to COM crystals. After exposure to COM for 48 hours, cell dedifferentiation were observed and more subsequent COM crystals could bind onto, mediated by Akt/GSK-3β/Snail signaling. L-carnitine attenuated this signaling, resulted in inhibition of cell dedifferentiation and reduction of subsequent COM crystals adhesion. Conclusions: COM attachment promotes subsequent COM crystals adhesion, by inducing cell dedifferentiation via Akt/GSK-3β/Snail signaling. L-carnitine partially abolishes cell dedifferentiation and resists COM crystals adhesion. L-carnitine, may be used as a potential therapeutic strategy against recurrence of urolithiasis.

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Nephroprotective potential of carnitine against glycerol and contrast-induced kidney injury in rats through modulation of oxidative stress, proinflammatory cytokines, and apoptosis

Abstract: Depending on the underlying kidney pathologies, the incidence of CM-induced nephropathy (CIN) increases. Therefore, this is the best model to represent clinically observed CIN.

Cited by 35 publications

References 69 publications

A new update for radiocontrast-induced nephropathy aggravated with glycerol in rats: the protective potential of epigallocatechin-3-gallate

A new update for radiocontrast-induced nephropathy aggravated with glycerol in rats: the protective potential of epigallocatechin-3-gallate

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

L-Carnitine Protects Renal Tubular Cells Against Calcium Oxalate Monohydrate Crystals Adhesion Through Preventing Cells From Dedifferentiation

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