scholarly journals Electroacupuncture Ameliorates Motor Dysfunction via Inhibiting p66Shc-Associated Oxidative Stress and Endoplasmic Reticulum Stress in Rats with Spinal Cord Injury

2020 ◽  
Author(s):  
Fusheng Zhao ◽  
Geng Wu ◽  
Yang Wu ◽  
Yunlong Bai ◽  
Yongjia Qiu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Endoplasmic Reticulum ◽  
Transcription Factor ◽  
Endoplasmic Reticulum Stress ◽  
Rating Scale ◽  
Motor Dysfunction ◽  
Cord Injury ◽  
Activating Transcription Factor

Abstract Background: Spinal cord injury (SCI) is a severe neurological disorder for which there is currently no effective treatment. Electroacupuncture (EA) is a type of traditional acupuncture combined with modern electrotherapy, which has been widely used and verified to have neuroprotective effects. The aim of this study was to evaluate the effects of EA stimulation on the repair of SCI and to investigate the possible mechanisms. Methods: Sprague-Dawley rats were randomly divided into sham, sham+EA, SCI and SCI+EA four groups. Rat motor function was assessed by the Basso, Beattie and Bresnahan locomotor rating scale, inclined plane test and footprint analysis. Histological alterations of spinal cords were examined with hematoxylin-eosin and Nissl staining. Oxidative stress was evaluated by measuring reactive oxygen species (ROS), glutathione (GSH), total antioxidant capacity (T-AOC), 3-nitrotyrosine (3-NT), and 4-hydroxynonenal (4-HNE) levels. The changes in p66Shc expression and endoplasmic reticulum stress (ERS) were detected to explore the involved mechanisms.Results: EA stimulation significantly improved rat motor functional recovery, reduced spinal cord lesion cavity and neuronal chromatolysis after SCI. Concomitantly, EA stimulation alleviated oxidative stress, as indicated by suppression of ROS production, increase in GSH and T-AOC levels and reduction of 3-NT and 4-HNE expression. Further, EA stimulation markedly eliminated the aberrant increase of p66Shc due to SCI in rats. More notably, EA stimulation was also able to attenuate ERS via down-regulation of glucose-regulated protein 78, activating transcription factor 4, C/EBP homologous protein, X-box binding protein 1 and activating transcription factor 6 expression in rat spinal cord tissues after SCI. Conclusions: These findings suggest that EA is a potential strategy for treatment of SCI, and the mechanism might be, at least in part, associated with mitigation of p66Shc-associated oxidative stress and ERS in rats.

scholarly journals Electroacupuncture ameliorates motor dysfunction via inhibiting p66Shc-mediated oxidative stress and endoplasmic reticulum stress in rats with spinal cord injury

2020 ◽  
Author(s):  
Fusheng Zhao ◽  
Geng Wu ◽  
Yang Wu ◽  
Yunlong Bai ◽  
Yongjia Qiu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Endoplasmic Reticulum ◽  
Transcription Factor ◽  
Endoplasmic Reticulum Stress ◽  
Rating Scale ◽  
Motor Dysfunction ◽  
Cord Injury ◽  
Activating Transcription Factor

Abstract Background: Spinal cord injury (SCI) is a severe neurological disorder for which there is currently no effective treatment. Electroacupuncture (EA) is a means of combining traditional acupuncture with modern electrotherapy, which has been widely used and verified to have neuroprotective effects. The aim of this study was to evaluate the effects of EA treatment on the repair of SCI and to investigate the possible mechanisms. Methods: Rats were randomly divided into sham, sham+EA, SCI and SCI+EA four groups after SCI model was established. Rat motor function was assessed by the Basso, Beattie and Bresnahan locomotor rating scale, inclined plane test and footprint analysis. Histological alterations were examined with hematoxylin-eosin and Nissl staining. Oxidative stress was evaluated by measuring reactive oxygen species (ROS), glutathione (GSH), total antioxidant capacity (T-AOC), 3-nitrotyrosine (3-NT), as well as 4-hydroxynonenal (4-HNE) levels. The expression of p66Shc and endoplasmic reticulum stress (ERS) were detected to explore the involved mechanisms.Results: EA treatment significantly improved motor functional recovery, reduced spinal cord lesion cavity and neuronal chromatolysis after SCI. Meanwhile, EA treatment alleviated oxidative stress, as indicated by suppression of ROS production, increase in GSH and T-AOC levels and reduction of 3-NT and 4-HNE expression. Further, EA stimulation markedly eliminated the aberrant increase of p66Shc due to SCI in rats. More notably, EA treatment also attenuated ERS via down-regulation of glucose-regulated protein 78, activating transcription factor 4, C/EBP homologous protein, X-box binding protein 1 and activating transcription factor 6 expression in rat spinal cord tissues after SCI. Conclusions: These findings suggest that EA is a potential strategy for treatment of SCI, and the mechanism might be, at least in part, associated with mitigation of p66Shc-mediated oxidative stress and ERS in rats.

Deletion of Endoplasmic Reticulum Stress-Induced CHOP Protects Microvasculature Post-Spinal Cord Injury

2012 ◽  
Vol 9 (4) ◽  
pp. 274-281 ◽  
Author(s):  
Janelle M. Fassbender ◽  
Sujata Saraswat-Ohri ◽  
Scott A. Myers ◽  
Mark J. Gruenthal ◽  
Richard L. Benton ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cord Injury

Necrostatin-1 Mitigates Endoplasmic Reticulum Stress After Spinal Cord Injury

2017 ◽  
Vol 42 (12) ◽  
pp. 3548-3558 ◽  
Author(s):  
Shuang Wang ◽  
Jin Wu ◽  
Yu-Zhe Zeng ◽  
Song-Song Wu ◽  
Guo-Rong Deng ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cord Injury

Activation of SIRT1 by Hyperbaric  Oxygenation Promotes Recovery of Motor Dysfunction in Spinal Cord Injury Rats

2020 ◽  
Author(s):  
Huiqiang Chen ◽  
Mengyu Yao ◽  
Zhibo Li ◽  
Ranran Xing ◽  
Cheng Zhang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Molecular Mechanisms ◽  
Hyperbaric Oxygenation ◽  
Rating Scale ◽  
Motor Dysfunction ◽  
Sprague Dawley ◽  
Inflammatory Cascade ◽  
Locomotor Function ◽  
Cord Injury

Abstract Background: Emerging evidence demonstrated that hyperbaric oxygenation (HBO) therapy improved the locomotor dysfunction following spinal cord injury (SCI). Sirtuin1(SIRT1) has been characterized as neuroprotection in nerve system. However, whether SIRT1 is involved in alleviation of locomotor function by HBO therapy is unclear. Methods: The Basso, Beattie Bresnahan (BBB) locomotor rating scale was used to evaluate the open-field locomotor function. Western blot, real-time quantitative reverse transcription polymerase chain reaction, SIRT1 activity assay and enzyme-linked immunosorbent assays were performed to explore the molecular mechanisms in adult Sprague-Dawley rats. Results: We found that series HBO therapy significantly improved the locomotor dysfunction and ameliorated the decrease mRNA, protein and activity of spinal cord SIRT1 induced by traumatic SCI injury in rats. In addition, intraperitoneal injection SIRT1 antagonist EX-527 abolished the beneficial effects of series HBO treatment on locomotor deficits and SIRT1 activity loss caused by traumatic SCI injury. However, the rats undergone both series HBO therapy and SIRT1 agonist SRT1720 got the higher BBB score than that undergone series HBO treatment only. Importantly, series HBO treatment following the traumatic SCI injury inhibited the inflammatory cascade and apoptosis-related protein, which was retained by EX-527 and enhanced by SRT1720. Furthermore, EX-527 blocked the enhanced induction of autophagy series with HBO application. Conclusion: These findings demonstrated a new mechanism for series HBO therapy involving activation of SIRT1 and subsequent modulation of inflammatory cascade, apoptosis and autophagy, which contributed to the recovery of motor dysfunction. Key words: HBO, SIRT1, motor dysfunction, inflammation, autophagy, apoptosis

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