Interleukin-1 receptor antagonist attenuates the severity of spinal cord ischemic injury in rabbits

Akuzawa, Satoshi; Kazui, Teruhisa; Shi, Enyi; Yamashita, Katsushi; Bashar, Abul Hasan Muhammad; Terada, Hitoshi

doi:10.1016/j.jvs.2008.04.011

Cited by 44 publications

(35 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…29 Absence of IL-1β inhibits lesion development and axonal plasticity and exerts positive effects on neurological outcome. 30 Blocking the IL-1 receptor suppresses microglial activation, promotes ventral horn neuron survival, 31 attenuates the severity of spinal cord 32 and promotes neurological recovery after SCI. 33 IL-18 is another kind of important proinflammatory cytokine after SCI.…”

Section: Discussionmentioning

confidence: 99%

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

et al. 2016

View full text Add to dashboard Cite

Study design: Randomized experimental study. Objectives: To investigate the molecular mechanisms of quercetin in spinal cord injury (SCI) rats. Setting: China. Methods: One hundred female Sprague-Dawley rats were randomly assigned into four groups: sham group, SCI group, SCI+Vehicle (Veh) group, and the SCI+Quercetin (Que) group. The influences of quercetin on proinflammatory cytokine levels, histological changes and locomotion scale were estimated. Results: SCI significantly promoted nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation and increased proinflammatory cytokine productions in the SCI group as compared with the sham group. Quercetin administration significantly decreased reactive oxygen species production, inhibited NLRP3 inflammasome activation and reduced inflammatory cytokine levels. Moreover, quercetin administration attenuated histopathology and promoted locomotion recovery. Conclusion: Quercetin can attenuate tissue damage and improve neurological function recovery, and the mechanism may be related to the inhibition of NLRP3 inflammasome activation.

show abstract

Section: Discussionmentioning

confidence: 99%

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

et al. 2016

View full text Add to dashboard Cite

show abstract

“…IL-1β-positive staining was observed in the ischemic regions of the cortex within 16-24 h after stroke (80). An elevated level of IL-1β can potentiate inflammation by activating microglia and induce the infiltration of peripheral leukocytes by increasing the expression of adhesion molecules on endothelial cells; these events are associated with worsening of the infarct severity and progressive neurodegeneration (81)(82)(83). In addition to its role as a pro-inflammatory mediator, IL-1β can also elevate the expression of other pro-inflammatory cytokines, such as IL-6 and TNF-α, which can be upregulated following cerebral ischemia (84).…”

Section: Role Of Cytokines In Cerebral Injury Following Ca and Resuscmentioning

confidence: 99%

Inflammatory mechanisms involved in brain injury following cardiac arrest and cardiopulmonary resuscitation

et al. 2016

View full text Add to dashboard Cite

Abstract. Cardiac arrest (CA) is a leading cause of fatality and long-term disability worldwide. Recent advances in cardiopulmonary resuscitation (CPR) have improved survival rates; however, the survivors are prone to severe neurological injury subsequent to successful CPR following CA. Effective therapeutic options to protect the brain from CA remain limited, due to the complexities of the injury cascades caused by global cerebral ischemia/reperfusion (I/R). Although the precise mechanisms of neurological impairment following CA-initiated I/R injury require further clarification, evidence supports that one of the key cellular pathways of cerebral injury is inflammation. The inflammatory response is orchestrated by activated glial cells in response to I/R injury. Increased release of danger-associated molecular pattern molecules and cellular dysfunction in activated microglia and astrocytes contribute to ischemia-induced cytotoxic and pro-inflammatory cytokines generation, and ultimately to delayed death of neurons. Furthermore, cytokines and adhesion molecules generated within activated microglia, as well as astrocytes, are involved in the innate immune response; modulate influx of peripheral immune and inflammatory cells into the brain, resulting in neurological injury. The present review discusses the molecular aspects of immune and inflammatory mechanisms in global cerebral I/R injury following CA and CPR, and the potential therapeutic strategies that target neuroinflammation and the innate immune system.

show abstract

“…Akuzawa et al, 2008;Gonzalez et al, 2007;Okada et al, 2004). Interestingly, 24 hours after SCI, 65.2% of genes were Exclusive Deletion of CD95L in Myeloid Cells Reduces Death of Neurons and Oligodendrocytes and Improves Functional Recovery after SCI (A and B) Twenty-four hours after transection-SCI, Fasl f/f;LysMcre mice exhibited lower amounts (A) of CD95L mRNA (n = 6/group) and (B) of caspase-3 activity (n = 4/group) compared to control littermates.…”

mentioning

confidence: 99%

CD95-Ligand on Peripheral Myeloid Cells Activates Syk Kinase to Trigger Their Recruitment to the Inflammatory Site

et al. 2010

View full text Add to dashboard Cite

Injury to the central nervous system initiates an uncontrolled inflammatory response that results in both tissue repair and destruction. Here, we showed that, in rodents and humans, injury to the spinal cord triggered surface expression of CD95 ligand (CD95L, FasL) on peripheral blood myeloid cells. CD95L stimulation of CD95 on these cells activated phosphoinositide 3-kinase (PI3K) and metalloproteinase-9 (MMP-9) via recruitment and activation of Syk kinase, ultimately leading to increased migration. Exclusive CD95L deletion in myeloid cells greatly decreased the number of neutrophils and macrophages infiltrating the injured spinal cord or the inflamed peritoneum after thioglycollate injection. Importantly, deletion of myeloid CD95L, but not of CD95 on neural cells, led to functional recovery of spinal injured animals. Our results indicate that CD95L acts on peripheral myeloid cells to induce tissue damage. Thus, neutralization of CD95L should be considered as a means to create a controlled beneficial inflammatory response.

show abstract

Interleukin-1 receptor antagonist attenuates the severity of spinal cord ischemic injury in rabbits

Abstract: Administration of IL-1ra attenuates spinal cord ischemic-reperfusion injury as evidenced by reducing both neuronal necrosis and apoptosis.

Cited by 44 publications

References 27 publications

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

Inflammatory mechanisms involved in brain injury following cardiac arrest and cardiopulmonary resuscitation

CD95-Ligand on Peripheral Myeloid Cells Activates Syk Kinase to Trigger Their Recruitment to the Inflammatory Site

Contact Info

Product

Resources

About