Experimental Analysis of Progressive Necrosis after Spinal Cord Trauma in the Rat: Etiological Role of the Inflammatory Response

1997 ◽  
Vol 143 (1) ◽  
pp. 141-152 ◽  
Author(s):  
Ziyin Zhang ◽  
Christopher J. Krebs ◽  
Lloyd Guth
Keyword(s):  
Spinal Cord ◽  
Inflammatory Response ◽  
Experimental Analysis ◽  
Spinal Cord Trauma ◽  
Etiological Role ◽  
Progressive Necrosis

scholarly journals The inflammatory response to a wheelchair half-marathon in people with a spinal cord injury - the role of autonomic function

2019 ◽  
Vol 37 (15) ◽  
pp. 1717-1724
Author(s):  
Sven P. Hoekstra ◽  
Christof A. Leicht ◽  
Yoshi-Ichiro Kamijo ◽  
Tokio Kinoshita ◽  
Ben T. Stephenson ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Autonomic Function ◽  
Cord Injury

scholarly journals CCL3 contributes to secondary damage after spinal cord injury

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Nicolas Pelisch ◽  
Jose Rosas Almanza ◽  
Kyle E. Stehlik ◽  
Brandy V. Aperi ◽  
Antje Kroner
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Lesion Size ◽  
Secondary Injury ◽  
Wild Type ◽  
Locomotor Recovery ◽  
Secondary Damage ◽  
Cord Injury

Abstract Background Secondary damage after spinal cord injury (SCI) is characterized by a cascade of events including hemorrhage, apoptosis, oxidative stress, and inflammation which increase the lesion size which can influence the functional impairment. Thus, identifying specific mechanisms attributed to secondary injury is critical in minimizing tissue damage and improving neurological outcome. In this work, we are investigating the role of CCL3 (macrophage inflammatory protein 1-α, MIP-1α), a chemokine involved in the recruitment of inflammatory cells, which plays an important role in inflammatory conditions of the central and peripheral nervous system. Methods A mouse model of lower thoracic (T11) spinal cord contusion injury was used. We assessed expression levels of CCL3 and its receptors on the mRNA and protein level and analyzed changes in locomotor recovery and the inflammatory response in the injured spinal cord of wild-type and CCL3−/− mice. Results The expression of CCL3 and its receptors was increased after thoracic contusion SCI in mice. We then examined the role of CCL3 after SCI and its direct influence on the inflammatory response, locomotor recovery and lesion size using CCL3−/− mice. CCL3−/− mice showed mild but significant improvement of locomotor recovery, a smaller lesion size and reduced neuronal damage compared to wild-type controls. In addition, neutrophil numbers as well as the pro-inflammatory cytokines and chemokines, known to play a deleterious role after SCI, were markedly reduced in the absence of CCL3. Conclusion We have identified CCL3 as a potential target to modulate the inflammatory response and secondary damage after SCI. Collectively, this study shows that CCL3 contributes to progressive tissue damage and functional impairment during secondary injury after SCI.

Role of histamine in posttraumatic spinal cord hyperemia and the luxury perfusion syndrome

1976 ◽  
Vol 44 (1) ◽  
pp. 16-20 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Thomas F. Doyle
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Related Phenomenon ◽  
Spinal Cord Trauma ◽  
Normal Range ◽  
Content Type ◽  
Lateral Funiculus ◽  
Receptor Sites ◽  
Luxury Perfusion

✓ The authors studied the effect of pretreatment of monkeys with antihistamines on hyperemia observed in the lateral funiculus of the spinal cord after severe experimental spinal cord trauma. After administration of Chlorpheniramine and Metiamide, the spinal cords were traumatized with a 600 gm-cm injury. Blood flow in the lateral funiculus at the injury site was then determined hourly for 6 hours. The blood flow at this site remained in the normal range at all times in all animals. Neither a hyperemia nor an ischemia could be demonstrated. This finding reaffirms the authors' previous observation that ischemia does not exist in the lateral funiculus after severe experimental spinal cord trauma, and explains the previous observation of hyperemia as a histamine-related phenomenon, easily blocked by the administration of Chlorpheniramine and Metiamide, potent antihistamines which together block both the H1 and H2 receptor sites.

Spinal cord injury by clip-compression induces anxiety and depression-like behaviours in female rats: The role of the inflammatory response

2019 ◽  
Vol 78 ◽  
pp. 91-104 ◽  
Author(s):  
Caroline Cunha do Espírito Santo ◽  
Fernando da Silva Fiorin ◽  
Jocemar Ilha ◽  
Marta Maria Medeiros Frescura Duarte ◽  
Tiago Duarte ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Female Rats ◽  
Anxiety And Depression ◽  
Cord Injury

scholarly journals Entinostat Improves Motor Function and Neuronal Damage Via Downregulating NLRP3 Inflammasome Activation After Spinal Cord Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Chen Dai ◽  
Bin Liu ◽  
Bibo Peng ◽  
Bo Qu ◽  
Jiezhi Lin ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Motor Function ◽  
Nlrp3 Inflammasome ◽  
Neuronal Damage ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Cord Injury

Background: Spinal cord injury (SCI), a major public health problem, has no effective treatment. A large number of studies have confirmed that histone deacetylases (HDACs) are involved in the physiologic processes that occur following SCI. We tried to uncover the potential neuroprotective role of entinostat (a class I HDAC inhibitor) in SCI.Methods: We conducted a study on a preclinical mouse model of SCI and OGD-induced neuronal damage to present the role of entinostat by the analysis of motor function, histopathologic damage, local NLRP3 inflammasome activation, and neuronal damage.Results: The results showed that entinostat suppressed HDAC activation (including HDAC1 and HDAC3 expression), improved the grip strength and BMS score, spinal edema, cell death, and local NLRP3 inflammasome activation in the spinal cord following SCI. Furthermore, entinostat significantly increased OGD-inhibited neuronal activity and decreased PI-positive cells, HDAC activation, caspase-1 activation, IL-1β and IL-18 levels, and NLRP3 expression.Conclusion: In summary, we first documented that entinostat improved the motor function, histopathologic damage, and local inflammatory response and NLRP3 inflammasome activation in the spinal cord following SCI and also presented the neuroprotective role of OGD-induced neuronal damage via the NLRP3 inflammasome. Thus, our study has the potential to reveal the interaction between the HDAC and NLRP3 inflammasome in the pathologic process as well as SCI and further promote the clinical indications of HDACi entinostat and clinical treatment for the inflammatory response after SCI.

scholarly journals Olprinone Attenuates the Acute Inflammatory Response and Apoptosis after Spinal Cord Trauma in Mice

PLoS ONE ◽  
2010 ◽  
Vol 5 (9) ◽  
pp. e12170 ◽  
Author(s):  
Emanuela Esposito ◽  
Emanuela Mazzon ◽  
Irene Paterniti ◽  
Daniela Impellizzeri ◽  
Placido Bramanti ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Inflammatory Response ◽  
Acute Inflammatory Response ◽  
Spinal Cord Trauma
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