Tnf-α inhibition by infliximab as a new target for the prevention of glycerol-contrast-induced nephropathy

Sarıtemur, Murat; Un, Harun; Çadırcı, Elif; Karakuş, Emre; Akpınar, Erol; Halıcı, Zekai; Uğan, Rüstem Anıl; Karaman, Adem; Atmaca, Hasan

doi:10.1016/j.etap.2015.01.002

Cited by 25 publications

(20 citation statements)

References 49 publications

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“…(k) Glycerol + RCM. Tubular necrosis and cast formation are more sever after combined injury (HE, 200x, from [36] with permission). (l, m) Combined model of diabetic nephropathy + RCM.…”

Section: Figurementioning

confidence: 99%

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Kiss

Hamar

2016

BioMed Research International

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Contrast-induced acute kidney injury (CI-AKI) can occur in 3–25% of patients receiving radiocontrast material (RCM) despite appropriate preventive measures. Often patients with an atherosclerotic vasculature have to receive large doses of RCM. Thus, animal studies to uncover the exact pathomechanism of CI-AKI are needed. Sensitive and specific histologic end-points are lacking; thus in the present review we summarize the histologic appearance of different rodent models of CI-AKI. Single injection of RCM causes overt renal damage only in rabbits. Rats and mice need an additional insult to the kidney to establish a clinically manifest CI-AKI. In this review we demonstrate that the concentrating ability of the kidney may be responsible for species differences in sensitivity to CI-AKI. The most commonly held theory about the pathomechanism of CI-AKI is tubular cell injury due to medullary hypoxia. Thus, the most common additional insult in rats and mice is some kind of ischemia. The histologic appearance is tubular epithelial cell (TEC) damage; however severe TEC damage is only seen if RCM is combined by additional ischemia. TEC vacuolization is the first sign of CI-AKI, as it is a consequence of RCM pinocytosis and lysosomal fusion; however it is not sensitive as it does not correlate with renal function and is not specific as other forms of TEC damage also cause vacuolization. In conclusion, histopathology alone is insufficient and functional parameters and molecular biomarkers are needed to closely monitor CI-AKI in rodent experiments.

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“…(k) Glycerol + RCM. Tubular necrosis and cast formation are more sever after combined injury (HE, 200x, from [36] with permission). (l, m) Combined model of diabetic nephropathy + RCM.…”

Section: Figurementioning

confidence: 99%

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Kiss

Hamar

2016

BioMed Research International

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“…In the light of these previous findings, we aimed to investigate the possible beneficial effects of infliximab pretreatment as a preventive strategy in an experimental model of sepsis induced by caecal ligation and puncture (CLP) with particular attention to the decreases in survival, mesenteric blood flow, contractile response of the aortic muscle to phenylephrine and as well as histopathological and biochemical injury in target vital organs such as liver, (Altintas et al 2016;Saritemur et al 2015). All animals were fasted overnight but allowed ad libitum access to drinking water one day before the operations.…”

Section: Introductionmentioning

confidence: 99%

Infliximab alleviates the mortality, mesenteric hypoperfusion, aortic dysfunction, and multiple organ damage in septic rats

Ozer

Göktaş

Kılınç

et al. 2017

Can. J. Physiol. Pharmacol.

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Keyword:infliximab, sepsis, survival, multiple organ dysfunction, vascular reactivity and mesenteric arterial blood flow https://mc06.manuscriptcentral.com/cjpp-pubs AbstractTumor necrosis factor-alpha (TNF-α) is a pivotal mediator that triggers inflammatory process, oxidative stress and multiple organ injury in sepsis. We investigated the effects of infliximab on survival, mesenteric artery blood flow (MBF), vascular reactivity, oxidative and inflammatory injuries in cecal ligation and puncture (CLP) induced sepsis. Wistar rats were divided into Sham, CLP, Sham+infliximab, CLP+infliximab subgroups. 24 hours before the operations rats were injected intraperitoneally with infliximab (7 mg/kg) or vehicle (saline; 1 mL/kg). 20 hours after operations MBF and phenylephrine responses of isolated aortic rings were measured. Tissue damages were examined biochemically and histopathologically. showed protective effects in sepsis due to its improvement effects on mesenteric perfusion, aortic function and its anti-inflammatory and antioxidative effects.

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“…Antioxidant protection preserves at the level of the glomerulus and reduces level of systemic inflammatory factors. 1 Although some prevention strategies exist, including adequate hydration of the patient, discontinuation of nephrotoxic drugs before CM administration and NAC, vitamins C and E treatment, 22 and some compounds such as infliximab 23 and simvastatin 24 have been shown to ameliorate CIN; there is no available standard prophylactic or therapeutic agent for this condition.…”

Section: Discussionmentioning

confidence: 99%

“…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%

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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Tnf-α inhibition by infliximab as a new target for the prevention of glycerol-contrast-induced nephropathy

Cited by 25 publications

References 49 publications

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Infliximab alleviates the mortality, mesenteric hypoperfusion, aortic dysfunction, and multiple organ damage in septic rats

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

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