Neuronal tumour necrosis factor-α and interleukin-1β expression in a porcine model of intracerebral haemorrhage: Modulation by U-74389G

Bimpis, Alexios; Papalois, Αpostolos; Voumvourakis, Konstantinos; Oláh, Orsolya; Tiszlavicz, Lazlo; Liapi, Charis

doi:10.1016/j.brainres.2015.04.034

Cited by 8 publications

(6 citation statements)

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“…Increasing evidence indicates that iNOS, COX-2, and various chemokines increase in response to activated IL-1β and TNF-α, leading to the inflammatory response as well as brain damage [45]. Numerous cytokines increase in the ICH brain, where many of those, such as IL-1β and TNFα, play a role in brain injury [8]. It was demonstrated in a model of spinal cord injury that the progression of tissue injury is regulated by IL-1β and TNF-α [46].…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies have shown that the inflammatory reaction plays a vital role in brain injury caused by ICH [6]. Tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) are secreted by neuronal cells and activated glial cells, such as microglia and astrocytes [7,8]. These cytokines ultimately destroy the blood-brain barrier (BBB) and cause neuronal death [9].…”

Section: Introductionmentioning

confidence: 99%

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Activation of PPAR-β/δ Attenuates Brain Injury by Suppressing Inflammation and Apoptosis in a Collagenase-Induced Intracerebral Hemorrhage Mouse Model

et al. 2020

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Brain injury has been proposed as the major cause of the poor outcomes associated with intracerebral hemorrhage (ICH). Emerging evidence indicates that the nuclear receptor, peroxisome proliferator-activated receptor β/δ (PPAR-β/δ), plays a crucial role in the pathological process of central nervous impairment. The present study was undertaken to evaluate the protective effects of PPAR-β/δ activation using a selective PPAR-β/δ agonist, GW0742, against brain injury after ICH in a mouse model. ICH was induced by intravenous injection of collagenase into the right caudate putamen. To examine the protective effect of PPAR-β/δ activation against ICH-induced brain injury, mice were either intraperitoneally injected with GW0742 (3 mg/kg, body weight) or saline (control group) 30 min before inducing ICH. Behavioral dysfunction was evaluated 24 and 72 h after injury. Then, all mice were killed to assess hematoma volume, brain water content, and blood-brain barrier (BBB) permeability. TUNEL and Nissl staining were performed to quantify the brain injury. The expression of PPAR-β/δ, interleukin (IL)-1β, tumor necrosis factor (TNF)-α, Bcl-2-related X-protein (Bax), and B-cell lymphoma 2 (Bcl-2) in the perihematomal area was examined by immunohistochemistry and western blotting analysis. Mice treated with GW0742 showed significantly less severe behavioral deficits compared to the control group, accompanied by increased expression of PPAR-β/δ and Bcl-2, and increased expression of IL-1β, TNF-α, and Bax decreased simultaneously in the GW0742-treated group. Furthermore, the GW0742-pretreated group showed significantly less brain edema and BBB leakage. Neuronal loss was attenuated, and the number of apoptotic neuronal cells in perihematomal tissues reduced, in the GW0742-pretreated group compared to the control group. However, the hematoma volume did not decrease significantly on day 3 after ICH. These results suggest that the activation of PPAR-β/δ exerts a neuroprotective effect on ICH-induced brain injury, possibly through anti-inflammatory and anti-apoptotic pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Activation of PPAR-β/δ Attenuates Brain Injury by Suppressing Inflammation and Apoptosis in a Collagenase-Induced Intracerebral Hemorrhage Mouse Model

et al. 2020

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“…In a porcine model of ICH, TNF-α and IL-1β expression measurements at 4 h after ICH revealed decreased TNF-α levels. However, the IL-1β levels did not decrease even 24 h after ICH 38 . TNF-α antibodies, such as CNTO 5048, reduced inflammation and improved functional outcome in a murine ICH model 39 .…”

Section: Discussionmentioning

confidence: 80%

PG2 for patients with acute spontaneous intracerebral hemorrhage: a double-blind, randomized, placebo-controlled study

Chen

et al. 2017

Sci Rep

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PG2 is an infusible polysaccharide extracted from Astragalus membranaceus, which is a Chinese herb traditionally used for stroke treatment. We investigated the effect of PG2 on patients with spontaneous acute intracerebral hemorrhage (ICH). A total of 61 patients with acute spontaneous ICH were randomized to either the treatment group (TG, 30 patients), which received 3 doses of PG2 (500 mg, IV) per week for 2 weeks, or the control group (CG, 31 patients), which received PG2 placebo. At 84 days after PG2 administration, the percentage of patients with a good Glasgow outcome scale (GOS 4–5) score in the TG was similar to that in the CG (69.0% vs. 48.4%; p = 0.2). The percentage of good mRS scores (0–2) in the TG was similar to that in the CG (62.1% vs. 45.2%; p = 0.3). In addition, no significant differences were seen when comparing differences in the C-reactive protein, erythrocyte sedimentation rate, interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α, and S100B levels between baseline and days 4, 7, and 14 after PG2 administration (all p > 0.05). The results are preliminary, necessitating a more thorough assessment.

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“…Another study showed that although TNF-α inhibitors can reduce the degree of brain edema, inflammation, and neurologic impairment, they do not alter hematoma volume (Lei et al, 2013). IL-1β produced by microglia/macrophages is also considered a key mediator of neuronal injury; some studies show that neuroprotection is associated with downregulation of IL-1β (Wu et al, 2010; Bimpis et al, 2015). To sum up, inflammation mediated by TLR4 signaling pathway lead to brain injury after ICH, which provides us with a potential therapeutic target of ICH.…”

Section: Secondary Brain Injurymentioning

confidence: 99%

Pathophysiological Mechanisms and Potential Therapeutic Targets in Intracerebral Hemorrhage

Shao

2019

Front. Pharmacol.

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Intracerebral hemorrhage (ICH) is a subtype of hemorrhagic stroke with high mortality and morbidity. The resulting hematoma within brain parenchyma induces a series of adverse events causing primary and secondary brain injury. The mechanism of injury after ICH is very complicated and has not yet been illuminated. This review discusses some key pathophysiology mechanisms in ICH such as oxidative stress (OS), inflammation, iron toxicity, and thrombin formation. The corresponding therapeutic targets and therapeutic strategies are also reviewed.

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Neuronal tumour necrosis factor-α and interleukin-1β expression in a porcine model of intracerebral haemorrhage: Modulation by U-74389G

Cited by 8 publications

References 64 publications

Activation of PPAR-β/δ Attenuates Brain Injury by Suppressing Inflammation and Apoptosis in a Collagenase-Induced Intracerebral Hemorrhage Mouse Model

Activation of PPAR-β/δ Attenuates Brain Injury by Suppressing Inflammation and Apoptosis in a Collagenase-Induced Intracerebral Hemorrhage Mouse Model

PG2 for patients with acute spontaneous intracerebral hemorrhage: a double-blind, randomized, placebo-controlled study

Pathophysiological Mechanisms and Potential Therapeutic Targets in Intracerebral Hemorrhage

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