Neuroprotective effects of infliximab in experimental spinal cord ischemic injury

Çağatay, Güven; Börcek, Alp Özgün; Cemil, Berker; Kurt, Gökhan; Yıldırım, Zühal; Uçankuş, NeşE Lortlar; Kılıç, Nedret; Çeviker, Necdet

doi:10.1016/j.jocn.2010.04.027

Cited by 32 publications

(22 citation statements)

References 22 publications

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“…Proinflammatory factors also play an important role in the pathogenesis of renal I/R injury through leukocyte activation and expression of adhesion molecules and cytokines. 14,30,31 Similarly, the increased production of TNF-α has a role in the pathophysiology of I/R injury. MPO, an abundant enzyme in phagocytes, has been implicated in the pathogenesis of various inflammatory diseases.…”

Section: Discussionmentioning

confidence: 99%

“…Infliximab (Remicade, Schering Plough Co., Innihannon, County Cork, Ireland) was administered intraperitoneally at a dose of 5 mg/kg. 14 All experimental procedures conform to the National Research Council guidelines 15 for the handling and care of laboratory animals. Moreover, all experimental procedures and protocols used in this investigation were reviewed and approved by the Animal Research Committee of Inonu University.…”

Section: Methods Experimental Groupsmentioning

confidence: 99%

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Protective Effect of Infliximab on Ischemia/Reperfusion-Induced Damage in Rat Kidney

et al. 2012

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Objective: To investigate the protective effect of infliximab on ischemia-reperfusion (I/R) injury of the rat kidney. Methods: Twenty-eight male Wistar albino rats were divided into four groups: sham-operated, I/R, I/R with infliximab administered before ischemia [I/R þ infliximab (bi)], and I/R with infliximab administered before reperfusion [I/R þ infliximab (br)]. After a right nephrectomy to produce damage, the left renal vessels were occluded for 60 min, followed by 24-h reperfusion in rats. Changes in the rat kidney were observed by measuring the tissue levels of malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH), and superoxide dismutase (SOD) and by evaluating hematoxylin-eosin (H&E)-stained and periodic acid-Schiff (PAS) sections. Results: The MDA and MPO levels in the I/R group were significantly higher than in the other groups (p < 0.05), and the SOD and GSH levels in the I/R þ infliximab (bi) and I/R þ infliximab (br) groups were significantly higher than in the I/R group (p < 0.05). However, histological examination revealed that the I/R þ infliximab (bi) group and the I/R þ infliximab (br) group had significantly fewer tubular changes and interstitial inflammatory cell infiltration than the I/R group. Conclusion: These results show that infliximab may protect against I/R injury in the rat I/R model.

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Section: Discussionmentioning

confidence: 99%

Section: Methods Experimental Groupsmentioning

confidence: 99%

Protective Effect of Infliximab on Ischemia/Reperfusion-Induced Damage in Rat Kidney

et al. 2012

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“…The body temperature of the rabbits was continuously monitored with a needle-type thermistor inserted into the paravertebral muscles at the L-3 and L-4 levels, and was maintained at approximately 38°C with a heating lamp and an underbody heating pad. The rabbit model of spinal cord ischemia and reperfusion described by Guven et al 10 was used to perform spinal cord ischemia and reperfusion. All rabbits were assigned a number from 1 to 18, randomly chosen by the senior author (G.K.), and all medication and surgical procedures were performed by a surgeon (E.C.)…”

Section: Animal Carementioning

confidence: 99%

Effects of curcumin on acute spinal cord ischemia-reperfusion injury in rabbits

Kurt

Yıldırım²,

Cemil

et al. 2014

SPI

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Object. The object of this study was to conduct a prospective, randomized, laboratory investigation of the neuroprotective effects of curcumin functionally, biochemically, and histologically in an experimental acute spinal cord ischemia-reperfusion injury on rabbits.Methods. Eighteen rabbits were randomly assigned to 1 of 3 groups: the sham group, the ischemia-reperfusion group, or the curcumin group. Spinal cord ischemia was induced by applying an infrarenal aortic cross-clamp for 30 minutes. At 48 hours after ischemia, neurological function was evaluated with modified Tarlov criteria. Biochemical changes in the spinal cord and plasma were observed by measuring levels of malondialdehyde (MDA), advanced oxidation protein products (AOPP), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitrite/nitrate, and tumor necrosis factor-a (TNF-a). Histological changes were examined with H & E staining. Immunohistochemical staining with antibodies against caspase-3 was performed to evaluate cell apoptosis after ischemia.Results. In the curcumin group, neurological outcome scores were statistically significantly better compared with the ischemia-reperfusion group. In the ischemia-reperfusion group, MDA, AOPP, and nitrite/nitrate levels were significantly elevated in the spinal cord tissue and the plasma by the induction of ischemia-reperfusion. The curcumin treatment significantly prevented the ischemia-reperfusion-induced elevation of nitrite/nitrate and TNF-a. In addition, the spinal cord tissue and the plasma SOD, GSH, and CAT levels were found to be preserved in the curcumin group and not statistically different from those of the sham group. Histological evaluation of the tissues also demonstrated a decrease in axonal damage, neuronal degeneration, and glial cell infiltration after curcumin administration.Conclusions. Although further studies including different dose regimens and time intervals are required, curcumin could attenuate a spinal cord ischemia-reperfusion injury in rabbits via reducing oxidative products and proinflammatory cytokines, as well as increasing activities of antioxidant enzymes and preventing apoptotic cell death. (http://thejns.org/doi/abs/10.3171/2013 keY WorDs • antioxidant • curcumin • ischemia-reperfusion injury • neuroprotection • oxidative stress • spinal cord injuryAbbreviations used in this paper: AOPP = advanced oxidation protein products; CAT = catalase; GSH = glutathione; MDA = malondialdehyde; SOD = superoxide dismutase; TBARS = thiobarbituric acid reactive substances; TNF = tumor necrosis factor.

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“…Infliximab is a chimeric antibody with a mouse variable fragment (Fv) and human antibody with immunoglobulin G1 (IgG1) and k constant regions [41,51,52] , which neutralizes the biological activity of TNF by binding to the soluble and trans-membrane forms of TNF and inhibits the binding of TNF with its receptors. The structure of Infliximab is similar to that of naturally occurring antibodies [41] .…”

Section: Infliximabmentioning

confidence: 99%

“…Infliximab has been shown to inhibit functional TNF-α activity in a variety of in vitro bioassays using human fibroblasts, endothelial cells, neutrophils, lymphocytes, and epithelial cells [56] . In vivo, infliximab is indicated for the treatment of rheumatologic, gastrointestinal, dermatologic, and chronic ocular diseases [51,57] . The role of infliximab has been shown to improve I/R injury in spinal injury models [51,58] and cardiac injury models [59,60] .…”

Section: Infliximabmentioning

confidence: 99%

Ischaemic/reperfusion injury: Role of infliximab

Bagul¹

2012

WJT

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Ischaemia/reperfusion (I/R) injury is an underlying complex interrelated patho-physiological process which effects the outcome of many clinical situations, in particular transplantation. Tumor necrosis factor (TNF)-α is a pleiotropic inflammatory cytokine; a trimeric protein encoded within the major histocompatibility complex which plays a pivotal role in this disease process. This review is based at looking into an update, particularly the new insights in the mechanisms of action of TNF antagonist such as infliximab. Infliximab may thus play a dual role in the field of transplantation where it might not only down regulate the I/R injury, it may also have a beneficial role in the reduction of acute rejection.

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Neuroprotective effects of infliximab in experimental spinal cord ischemic injury

Cited by 32 publications

References 22 publications

Protective Effect of Infliximab on Ischemia/Reperfusion-Induced Damage in Rat Kidney

Protective Effect of Infliximab on Ischemia/Reperfusion-Induced Damage in Rat Kidney

Effects of curcumin on acute spinal cord ischemia-reperfusion injury in rabbits

Ischaemic/reperfusion injury: Role of infliximab

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