Effects of infliximab against carbon tetrachloride-induced intestinal injury via lipid peroxidation and apoptosis

Pergel, Ahmet; Tümkaya, Levent; Çolakoğlu, Muhammed Kadri; Demiral, Gökhan; Kalcan, Süleyman; Özdemir, Ali; Yılmaz, Adnan

doi:10.1177/0960327119867758

Cited by 10 publications

(5 citation statements)

References 34 publications

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“…The ndings showed that continuous cold stimulation induces an increase in HSP70 protein expression but not HSP90. It has been suggested that an essential indicator of intestinal injury is the apoptosis of intestinal epithelial cells [37].…”

Section: Discussionmentioning

confidence: 99%

Effect of chronic cold stress on gut microbial diversity, intestinal inflammation and pyroptosis in mice

Lv,

Xia,

et al. 2024

J Physiol Biochem

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Hypothermia is an essential environmental factor in gastrointestinal diseases, but the main molecular mechanisms of pathogenesis remain unclear. The current study sought to better understand how chronic cold stress affects gut damage and its underlying mechanisms. In this work, to establish chronic cold stress (CS)-induced intestinal injury model, mice were subjected to prolonged cold exposure (4°C) for 3 h per day for 3 weeks. Our results indicated that CS led to gut injury via inducing changes of heat shock proteins 70 (HSP70) and apoptosis-related (caspases-3, Bax and Bcl-2) proteins; enhancing expression of intestinal tight-related (ZO-1 and occludin) proteins; promoting releases of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), high mobility group box 1 (HMGB1), interleukin1β (IL-1β), IL-18 and IL-6 in ammatory mediators in the ileum; and altering gut microbial diversity. Furthermore, persistent cold exposure resulted in the cleavage of pyroptosis-related Gasdermin D (GSDMD) protein by regulating the NLRP3/ASC/caspase-1 and caspase-11 pathway, and activation of toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways, which are strongly associated with changes in gut microbiota diversity. Taken together, these investigations provide new insights into the increased risk of intestinal disorders at extremely low temperatures and establish a theoretical foundation for the advancement of novel pharmaceutical interventions targeting cold-related ailments.

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Section: Discussionmentioning

confidence: 99%

Effect of chronic cold stress on gut microbial diversity, intestinal inflammation and pyroptosis in mice

Lv,

Xia,

et al. 2024

J Physiol Biochem

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“…The drug's inability to differentiate between sTNF and tmTNF poses challenges, inhibiting baseline activity and causing adverse effects [69]. Exogenous TNF blockers, including etanercept, may increase the risk of serious infections and cancer according to a meta-analysis of clinical trials comparing TNF-binding medications like etanercept and infliximab [73]. Etanercept, in placebo-controlled trials, demonstrated a 35% infection rate over the therapy course, associated with serious bacterial, viral, and fungal infections [69].…”

Section: Tnf As a Therapeutic Targetmentioning

confidence: 99%

The Role of Tnf and Soluble Tnf Receptors (TNFR1/2) as Therapeutic Targets for Inflammation Secondary to Intracerebral Stroke and Hemorrhage

Alshaibi,

Ekanayake,

Barlow

et al. 2024

Preprint

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Most neurodegenerative diseases, including Alzheimer's disease, ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage are associated with inflammation. Tumor necrosis factor (TNF) is a pleiotropic pro-inflammatory cytokine that regulates cerebral infarction in stroke pathology, and its action is influenced by the bioavailability of its membrane-bound receptors, TNFR1 and TNFR2, and microglial activation. During the initial onset of these diseases, the soluble variant of the cytokine presents with prolonged and excessive activation of TNFR1, resulting in cell death and long-term neurological impairments. Therapeutic interventions for neurodegenerative diseases have targeted TNF to limit the onset of neuroinflammation. First-generation therapeutics have been demonstrated to inhibit membrane-bound TNF to TNFR2 receptor binding, resulting in severe side effects such as infections and cancer. As such, second-generation drugs, including XPro1595, have been developed to selectively inhibit soluble TNF and impede the effects of TNFR1 while still allowing for TNFR2 activation. Early results in murine TBI models demonstrate reduced glial reactivity by 50%, reduced dendritic degeneration by 30%, increased plasticity by 15%, and improved functional outcomes by 20% post-TBI. This scoping review of TNF receptors in various neurodegenerative diseases seeks to evaluate current and future therapeutic strategies as well as highlight potential strategies to eliminate confounding variables present in the current literature.

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“…It was shown to result in histopathological findings such as vascular congestion, infiltration, and vacuolar degeneration in cells in the liver (1). Moreover, it induces oxidative damage by increasing the amounts of malondialdehyde (MDA), which is an oxidative stress marker, in the intestine and the lung, as well as increasing the number of cells marked by the TUNEL method, which indicates necrotic cells (5,6).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of The Effects of Dexmedetomidine against Carbontetracloride-Induced Nephrotoxicity via Oxidative Stress and Apoptosis

Dil,

Tumkaya,

Mercantepe

et al. 2023

Med Sci Discov

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Objective: The objective of this work is to investigate the histological and biochemical consequences of administering Dexmedetomidine (DEX), an alpha-2 adrenergic receptor agonist with notable sedative qualities as well as antioxidant and anti-inflammatory characteristics, in the context of Carbon tetrachloride (CCl4)-induced kidney injury. Materials and Methods: The experimental design involved the random allocation of 30 Sprague-Dawley rats into three distinct groups. The experimental group designated as Group 1 received a single intraperitoneal administration of 1ml of saline solution containing 0.09% NaCl. Group 2 received an intraperitoneal injection of carbon tetrachloride (CCl4) at a dosage of 2 milliliters per kilogram. Group 3, referred to as the CCl4+Dexmedetomidine group, received a solitary intraperitoneal (i.p.) dosage of 100 µg/kg dexmedetomidine one hour before the intraperitoneal administration of 2mL/kg CCl4. Results: Extensive necrosis and debris accumulation were observed in the tubules, particularly in the proximal tubules, within the CCl4-applied group. An elevation in malondialdehyde (MDA) concentrations and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) positivity, along with a reduction in glutathione (GSH) levels, was found in the renal tissues of the CCl4 experimental group as compared to the control group. In contrast, the CCl4+DEX group exhibited a reduction in the quantity of necrotic tubular cells, levels of MDA, and TUNEL positive. Additionally, there was an elevation in GSH levels compared to the group treated with CCl4 alone. Conclusions: The administration of dexmedetomidine has been observed to potentially provide a protective effect against renal damage induced by CCl4. This phenomenon could potentially be linked to the modulation of tissue oxidative stress markers and the attenuation of apoptotic rate. The findings of our investigation provide evidence in favour of the utilization of dexmedetomidine as a promising therapeutic drug for mitigating renal injury.

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Effects of infliximab against carbon tetrachloride-induced intestinal injury via lipid peroxidation and apoptosis

Cited by 10 publications

References 34 publications

Effect of chronic cold stress on gut microbial diversity, intestinal inflammation and pyroptosis in mice

Effect of chronic cold stress on gut microbial diversity, intestinal inflammation and pyroptosis in mice

The Role of Tnf and Soluble Tnf Receptors (TNFR1/2) as Therapeutic Targets for Inflammation Secondary to Intracerebral Stroke and Hemorrhage

Evaluation of The Effects of Dexmedetomidine against Carbontetracloride-Induced Nephrotoxicity via Oxidative Stress and Apoptosis

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