The neuroprotective effects of adalimumab on rats with experimental peripheral nerve injury: an electron microscopic and biochemical study.

Polat, Ersin; Dağlıoğlu, Ergün; Menekşe, Güner; Dike, M Serdar; Özdöl, Çağatay; Türk, Cezmi Çağrı; Yıldırım, Ali Erdem; Alagöz, Fatíh; Dalgıç, Ali; Belen, Deniz

doi:10.5505/tjtes.2015.54358

Cited by 4 publications

(6 citation statements)

References 19 publications

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“…This dosage and treatment regimen was decided according to the literature. [6] The animals tolerated this dosage well without any important side effects.…”

Section: Groupsmentioning

confidence: 88%

Ameliorating Effects of Adalimumab on Rabbits with Experimental Cerebral Vasospasm After Subarachnoid Hemorrhage

Toğuşlu

Erdi

Arac

et al. 2020

Ulus Travma Acil Cerrahi Derg

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BACKGROUND: Adalimumab (ADA), which is a new-generation recombinant human monoclonal antibody for tumor necrosis factor α (TNFα), has strong anti-inflammatory effects. The role of enhanced inflammation is well established for the development and progression of cerebral vasospasm. Investigated in the present study is the probable ameliorating and neuroprotective effects of ADA in rabbits using a cerebral vasospasm model with biochemical and histopathological methods. METHODS: Thirty male New-Zealand white rabbits were randomly divided into control, subarachnoid hemorrhage (SAH) only and SAH plus ADA treatment groups. SAH was established as a single cisterna magna autologous arterial blood injection. ADA treatment was started just after intracisternal blood injection and continued for 72 hours once a day. The animals were sacrificed 72 hours after the induction of SAH, serum and brainstem tissue obtained for investigations. RESULTS: Brainstem tissue and plasma levels of tumor necrosis factor-alpha and Interleukin-1β, brainstem tissue Matrix metalloproteinase-9 levels increased after SAH and partly decreased after treatment. Plasma levels of brain-derived neurotrophic factor decreased after SAH and partly restored after treatment. ADA treatment significantly increased the mean cross-sectional area of the vasospastic basilar arteries, reduced the basilar artery wall thickness and also ameliorates enhanced endothelial apoptosis. CONCLUSION: Findings obtained in this study suggest that ADA is an effective neuroprotective agent for ameliorating cerebral vasospasm in experimental rabbit vasospasm.

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“…This dosage and treatment regimen was decided according to the literature. [6] The animals tolerated this dosage well without any important side effects.…”

Section: Groupsmentioning

confidence: 88%

Ameliorating Effects of Adalimumab on Rabbits with Experimental Cerebral Vasospasm After Subarachnoid Hemorrhage

Toğuşlu

Erdi

Arac

et al. 2020

Ulus Travma Acil Cerrahi Derg

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“…For predicting the candidate e cient treatment against SNI and the associated concurrent diseases, this study used DGIdb database for determining the therapeutic agents showing effects on reversing the abnormal up-regulation of SNI-associated hub genes. Tumor necrosis factor-alpha (TNF-α) is suggested to exert a vital part during demyelination and apoptosis, while blocking its expression enhances neural healing (54). According to previous reports, TNF-α antagonists are effective on Schwann cells and axons within SNI, and TNF-α is related to the modulation of axonal regeneration (55).…”

Section: Discussionmentioning

confidence: 99%

“…An increasing number of epidemiological studies have suggested that, the anti-TNF-α therapies, including adalimumab, etanercept and adalimumab, are utilized to treat different peripheral nerve diseases, including chronic in ammatory demyelinating polyneuropathy, Miller Fisher syndrome, Guillain-Barré syndrome, mononeuropathy multiplex, multifocal motor neuropathy accompanied by conduction block, and axonal sensorimotor polyneuropathy (56). Adalimumab was detected as the e cient neuroprotective drug to heal the nerves in PNI model of rats, particularly in the early phase (54). Trastuzumab have also been reported to enhance peripheral nerve regeneration following repair from acute and chronic PNI (57,58).…”

Section: Discussionmentioning

confidence: 99%

Gene Correlation Network Analysis To Identify Regulatory Factors In Sciatic Nerve Injury

Ling

et al. 2021

Preprint

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Background: Sciatic nerve injury (SNI), which frequently occurs under the traumatic hip and hip fracture dislocation, induces serious complications such as motor and sensory loss, muscle atrophy, or even disabling. The present work aimed to determine the regulating factors and gene network related to the SNI pathology.Methods: Sciatic nerve injury dataset GSE18803 with 24 samples was randomly divided into adult group and neonate group. We performed weighted gene co-expression network analysis (WGCNA) to identify modules associated with SNI in the two groups. Moreover, differentially expressed genes (DEGs) were determined from every group, separately. Subsequently, co-expression network, protein-protein interaction (PPI) network, enrichment analysis and gene set enrichment analysis (GSEA) were integrated to identify hub genes and associated pathways. GSE30165 was used as the test set for investigating the hub gene involvement within SNI. Finally, we employed DGIdb for predicting the possible therapeutic agents leading to the abnormal up-regulation of hub genes.Results: 14 SNI status modules and 97 DEGs were identified in adult group, while 15 modules and 21 DEGs in neonate group. A total of 12 hub genes was overlapping from co-expression and PPI network. After the results from both test and training sets were overlapped, we verified that the ten real hub genes showed remarkably up-regulation within SNI. According to functional enrichment of DEGs, the above genes participated in the immune effector process, inflammatory responses, the antigen processing and presentation, and the phagocytosis. GSEA also supported that gene sets with the highest significance was mostly related to the cytokine-cytokine receptor interaction.Conclusions: The gene expression network is determined in the present work based on the related regulating factors within SNI, which sheds more lights on SNI pathology and offers the possible biomarkers and therapeutic targets in subsequent research.

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“…Low-dose adalimumab (5 mg/kg/day) was observed to exhibit ameliorative effects on the intestinal injury induced through H/R in the present study, whereas the high dose of adalimumab (50 mg/kg/day) did not exhibit similar properties. Polat et al also showed that low-dose adalimumab (5 mg/kg) has beneficial effects on ischemia/reperfusion-induced peripheral nerve injury, whereas a high dose of adalimumab (50 mg/kg) had no similar effects [10]. In the previous studies with rats, adalimumab was used at different low doses such as 5 mg/kg and 10 mg/kg, and at a higher dose such as 50 mg/kg [9,10,24].…”

Section: Discussionmentioning

confidence: 99%

“…Several experimental studies investigated the effectiveness of adalimumab at different doses. In those studies, adalimumab as an anti-inflammatory agent significantly decreased nerve tissue lipid peroxidation in rats with experimental peripheral nerve injury, and it had beneficial effects on experimentally induced acute pancreatitis in rats [9,10]. The current study aimed to determine dose-dependent effects of adalimumab on intestinal injury induced with H/R in neonatal rat pups.…”

Section: Introductionmentioning

confidence: 92%

Dose-dependent effects of adalimumab in neonatal rats with hypoxia/reoxygenation-induced intestinal damage

Kocamaz

Özdemir

Türk

et al. 2020

Bosn J of Basic Med Sci

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Tumor necrosis factor-alpha (TNF-α) has an important role in hypoxia/reoxygenation (H/R)-induced intestinal damage. It was shown that blocking TNF-α with infliximab has beneficial effects on experimental necrotizing enterocolitis and hypoxic intestinal injury. However, there is no data about the effect of adalimumab on H/R-induced intestinal damage. Therefore, we aimed to determine potential dose-dependent benefits of adalimumab in such damage in neonatal rats. Wistar albino rat pups were assigned to one of the four groups: control group, hypoxia group, low-dose adalimumab (5 mg/kg/day) treated group (LDAT), and high-dose adalimumab (50 mg/kg/day) treated group (HDAT). On the fourth day of the experiment, all rats except for the control group were exposed to H/R followed by euthanasia. Malondialdehyde (MDA), myeloperoxidase (MPO), TNF-α, total antioxidant capacity (TAC), and total oxidant capacity (TOC) were measured in intestinal tissue. TAC and TOC values were used to calculate the oxidative stress index (OSI). Histopathological injury scores (HIS) were also evaluated in the tissue samples. MDA levels were significantly lower in the LDAT and HDAT groups (p < 0.001). TNF-α levels were significantly lower in the LDAT group (p < 0.001). OSI was significantly higher in the H/R group than in the control and LDAT groups (p < 0.001). Mean HIS values in the LDAT group were significantly lower than those in the H/R and HDAT groups (p < 0.001). This experimental study showed that low-dose adalimumab appears to have a beneficial effect on intestinal injury induced with H/R in neonatal rats.

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The neuroprotective effects of adalimumab on rats with experimental peripheral nerve injury: an electron microscopic and biochemical study.

Cited by 4 publications

References 19 publications

Ameliorating Effects of Adalimumab on Rabbits with Experimental Cerebral Vasospasm After Subarachnoid Hemorrhage

Ameliorating Effects of Adalimumab on Rabbits with Experimental Cerebral Vasospasm After Subarachnoid Hemorrhage

Gene Correlation Network Analysis To Identify Regulatory Factors In Sciatic Nerve Injury

Dose-dependent effects of adalimumab in neonatal rats with hypoxia/reoxygenation-induced intestinal damage

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