Protective effects of erythropoietin in traumatic spinal cord injury by inducing the Nrf2 signaling pathway activation

2014 ◽  
Vol 76 (5) ◽  
pp. 1228-1234 ◽  
Author(s):  
Wei Jin ◽  
Xing Ming ◽  
Xiaoshan Hou ◽  
Tiansheng Zhu ◽  
Baoyu Yuan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Signaling Pathway ◽  
Traumatic Spinal Cord Injury ◽  
Protective Effects ◽  
Pathway Activation ◽  
Nrf2 Signaling Pathway ◽  
Cord Injury

scholarly journals Methylprednisolone Induces Neuro-Protective Effects via the Inhibition of A1 Astrocyte Activation in Traumatic Spinal Cord Injury Mouse Models

2021 ◽  
Vol 15 ◽  
Author(s):  
Hong-jun Zou ◽  
Shi-Wu Guo ◽  
Lin Zhu ◽  
Xu Xu ◽  
Jin-bo Liu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Mouse Models ◽  
Neuronal Cells ◽  
Neurological Function ◽  
Traumatic Spinal Cord Injury ◽  
Protective Effects ◽  
Astrocyte Activation ◽  
Cord Injury

Traumatic spinal cord injury (TSCI) leads to pathological changes such as inflammation, edema, and neuronal apoptosis. Methylprednisolone (MP) is a glucocorticoid that has a variety of beneficial effects, including decreasing inflammation and ischemic reaction, as well as inhibiting lipid peroxidation. However, the efficacy and mechanism of MP in TSCI therapy is yet to be deciphered. In the present study, MP significantly attenuated the apoptotic effects of H2O2 in neuronal cells. Western blot analysis demonstrated that the levels of apoptotic related proteins, Bax and cleaved caspase-3, were reduced while levels of anti-apoptotic Bcl-2 were increased. In vivo TUNEL assays further demonstrated that MP effectively protected neuronal cells from apoptosis after TSCI, and was consistent with in vitro studies. Furthermore, we demonstrated that MP could decrease expression levels of IBA1, Il-1α, TNFα, and C3 and suppress A1 neurotoxic reactive astrocyte activation in TSCI mouse models. Neurological function was evaluated using the Basso Mouse Scale (BMS) and Footprint Test. Results demonstrated that the neurological function of MP-treated injured mice was significantly increased. In conclusion, our study demonstrated that MP could attenuate astrocyte cell death, decrease microglia activation, suppress A1 astrocytes activation, and promote functional recovery after acute TSCI in mouse models.

Geniposide exerts protective effects on spinal cord injury in rats by inhibiting the IKKs/NF-κB signaling pathway

2021 ◽  
Vol 100 ◽  
pp. 108158
Author(s):  
Yuying Li ◽  
Huiping Qiu ◽  
Shuihong Yao ◽  
Qunfeng Li ◽  
Yuemin Ding ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Signaling Pathway ◽  
Protective Effects ◽  
Cord Injury

A Pivotal Role of the Nrf2 Signaling Pathway in Spinal Cord Injury: A Prospective Therapeutics Study

2020 ◽  
Vol 19 (3) ◽  
pp. 207-219
Author(s):  
Saeed Samarghandian ◽  
Ali Mohammad Pourbagher-Shahri ◽  
Milad Ashrafizadeh ◽  
Haroon Khan ◽  
Fatemeh Forouzanfar ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Signaling Pathway ◽  
Experimental Studies ◽  
Main Role ◽  
Related Factor ◽  
Nrf2 Signaling Pathway ◽  
Cord Injury ◽  
Anti Inflammatory ◽  
The Impact

The nuclear erythroid 2-related factor 2 (Nrf2) signaling pathway has a main role against oxidative stress and inflammation. Spinal Cord Injury (SCI) leads to the high secretion of inflammatory cytokines and reactive oxygen species, which disturbs nervous system function and regeneration. Several studies have indicated that the activation of the Nrf2 signaling pathway may be effective against inflammation after SCI. The experimental studies have indicated that many chemical and natural agents act as Nrf2 inducer, which inhibits the SCI progression. Thus, the finding of novel Nrf2- inducer anti-inflammatory agents may be a valuable approach in drug discovery. In the present review, we discussed the Nrf2 signal pathway and crosstalk with the NF-κB pathway and also the impact of this pathway on inflammation in animal models of SCI. Furthermore, we discussed the regulation of Nrf2 by several phytochemicals and drugs, as well as their effects on the SCI inhibition. Therefore, the current study presented a new hypothesis of the development of anti-inflammatory agents that mediate the Nrf2 signaling pathway for treating the SCI outcomes.

4:5342. The protective effects of a novel adenosine A2a analogue following traumatic spinal cord injury in a rat model

2005 ◽  
Vol 5 (4) ◽  
pp. S22
Author(s):  
Eric Francke ◽  
John Thaller ◽  
Brian Leo ◽  
D. Greg Anderson ◽  
Francis Shen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Rat Model ◽  
Traumatic Spinal Cord Injury ◽  
Protective Effects ◽  
Cord Injury ◽  
Adenosine A2a

Effects of hyperbaric oxygen therapy on long-tract neuronal conduction in the acute phase of spinal cord injury

1981 ◽  
Vol 55 (4) ◽  
pp. 501-510 ◽  
Author(s):  
Alfred C. Higgins ◽  
Robert D. Pearlstein ◽  
John B. Mullen ◽  
Blaine S. Nashold
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Hyperbaric Oxygen ◽  
Absolute Pressure ◽  
Traumatic Spinal Cord Injury ◽  
Protective Effects ◽  
Content Type ◽  
Spinal Cord Evoked Potentials ◽  
Cord Injury ◽  
Fine Print

✓ To study the acute effects of hyperbaric oxygen ventilation (HBO) on long-tract function following spinal cord trauma, the authors employed a technique for monitoring spinal cord evoked potentials (SCEP) as an objective measure of translesion neuronal conduction in cats subjected to transdural impact injuries of the spinal cord. Control animals subjected to injuries of a magnitude of 400 or 500 gm-cm occasionally demonstrated spontaneous return of translesion SCEP within 2 hours of injury when maintained by pentobarbital anesthesia and by ventilation with ambient room air at 1 atmosphere absolute pressure (1 ATA). Animals sustaining corresponding injuries but receiving immediate treatment with HBO at 2 ATA for a period of 3 hours following impact demonstrated variable responses to this treatment modality. Animals sustaining injuries of 400 gm-cm magnitude showed recovery of translesion SCEP in four of five cases, while animals sustaining injuries of 500 gm-cm magnitude responded to HBO treatment by recovery of SCEP no more frequently than did control animals. When the onset of HBO therapy was delayed by 2 hours following impact, there appeared to be no demonstrable protective effect on long-tract neuronal conduction mediated by HBO alone. The observations suggest that HBO treatments can mediate preservation of marginally injured neuronal elements of the spinal cord long tracts during the early phases of traumatic spinal cord injury. These protective effects may be based upon the reversal of focal tissue hypoxia, or by reduction of tissue edema, or possibly by both of these mechanisms. Increasing magnitudes of impact force and delay in the onset of HBO treatment markedly diminished the protective effects of HBO on long-tract neuronal conduction following traumatic spinal cord injury.

Sign in / Sign up

Export Citation Format

Share Document