scholarly journals HDAC6 Regulates the Chaperone-Mediated Autophagy to Prevent Oxidative Damage in Injured Neurons after Experimental Spinal Cord Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Min Su ◽  
Huaqing Guan ◽  
Fan Zhang ◽  
Yarong Gao ◽  
Xiaomei Teng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Potential Role ◽  
Mechanical Trauma ◽  
Ros Generation ◽  
Histone Deacetylase 6 ◽  
Cord Injury ◽  
Chaperone Mediated Autophagy

Hypoxia-ischemia- (HI-) induced oxidative stress plays a role in secondary pathocellular processes of acute spinal cord injury (SCI) due to HI from many kinds of mechanical trauma. Increasing evidence suggests that the histone deacetylase-6 (HDAC6) plays an important role in cell homeostasis in both physiological and abnormal, stressful, pathological conditions. This paper found that inhibition of HDAC6 accelerated reactive oxygen species (ROS) generation and cell apoptosis in response to the HI. Deficiency of HDAC6 hindered the chaperone-mediated autophagy (CMA) activity to resistance of HI-induced oxidative stress. Furthermore, this study provided the experimental evidence for the potential role of HDAC6 in the regulation of CMA by affecting HSP90 acetylation. Therefore, HDAC6 plays an important role in the function of CMA pathway under the HI stress induced by SCI and it may be a potential therapeutic target in acute SCI model.

scholarly journals Potential role of oxidative stress on the prescription of rehabilitation interventions in spinal cord injury

Spinal Cord ◽  
2013 ◽  
Vol 51 (9) ◽  
pp. 656-662 ◽  
Author(s):  
T Lam ◽  
Z Chen ◽  
M M Sayed-Ahmed ◽  
A Krassioukov ◽  
A A Al-Yahya
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Potential Role ◽  
Cord Injury

scholarly journals Effects of Polyphenols on Oxidative Stress, Inflammation, and Interconnected Pathways during Spinal Cord Injury

2022 ◽  
Vol 2022 ◽  
pp. 1-34
Author(s):  
Sajad Fakhri ◽  
Fatemeh Abbaszadeh ◽  
Seyed Zachariah Moradi ◽  
Hui Cao ◽  
Haroon Khan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Secondary Metabolites ◽  
Potential Role ◽  
Therapeutic Agents ◽  
Cord Injury ◽  
Potential Alternative ◽  
Preclinical And Clinical Studies

Despite the progression in targeting the complex pathophysiological mechanisms of neurodegenerative diseases (NDDs) and spinal cord injury (SCI), there is a lack of effective treatments. Moreover, conventional therapies suffer from associated side effects and low efficacy, raising the need for finding potential alternative therapies. In this regard, a comprehensive review was done regarding revealing the main neurological dysregulated pathways and providing alternative therapeutic agents following SCI. From the mechanistic point, oxidative stress and inflammatory pathways are major upstream orchestras of cross-linked dysregulated pathways (e.g., apoptosis, autophagy, and extrinsic mechanisms) following SCI. It urges the need for developing multitarget therapies against SCI complications. Polyphenols, as plant-derived secondary metabolites, have the potential of being introduced as alternative therapeutic agents to pave the way for treating SCI. Such secondary metabolites presented modulatory effects on neuronal oxidative stress, neuroinflammatory, and extrinsic axonal dysregulated pathways in the onset and progression of SCI. In the present review, the potential role of phenolic compounds as critical phytochemicals has also been revealed in regulating upstream dysregulated oxidative stress/inflammatory signaling mediators and extrinsic mechanisms of axonal regeneration after SCI in preclinical and clinical studies. Additionally, the coadministration of polyphenols and stem cells has shown a promising strategy for improving post-SCI complications.

Protective role of β-carotene against oxidative stress and neuroinflammation in a rat model of spinal cord injury

2018 ◽  
Vol 61 ◽  
pp. 92-99 ◽  
Author(s):  
Lihui Zhou ◽  
Lian Ouyang ◽  
Shuangzhi Lin ◽  
Song Chen ◽  
YingJie Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Rat Model ◽  
Protective Role ◽  
Cord Injury ◽  
Β Carotene

scholarly journals Catalpol Protects Against Spinal Cord Injury in Mice Through Regulating MicroRNA-142-Mediated HMGB1/TLR4/NF-κB Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Hougang Xia ◽  
Dandan Wang ◽  
Xiaohui Guo ◽  
Kaidi Wu ◽  
Fuwei Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Inflammatory Factors ◽  
Tunel Staining ◽  
Ros Generation ◽  
Bv2 Cells ◽  
Cord Injury ◽  
Oxidative Response

Background: Spinal cord injury (SCI) is a devastating condition that leads to paralysis, disability and even death in severe cases. Inflammation, apoptosis and oxidative stress in neurons are key pathogenic processes in SCI. Catalpol (CTP), an iridoid glycoside extracted from Rehmannia glutinosa, has many pharmacological activities, such as anti-inflammatory, anti-oxidative and anti-apoptotic properties.Purpose: Here, we investigated whether CTP could exert neuroprotective effects against SCI, and explored the underlying mechanism involved.Methods: SCI was induced by a weight-drop device and treated with CTP (10 mg and 60 mg/kg). Then the locomotor function of SCI mice was evaluated by the BBB scores, spinal cord edema was measured by the wet/dry weight method, oxidative stress markers and inflammatory factors were detected by commercial kits and neuronal death was measured by TUNEL staining. Moreover, the microRNA expression profile in spinal cords from mice following SCI was analyzed using miRNA microarray. In addition, reactive oxygen species (ROS) generation, inflammatory response and cell apoptosis were detected in murine microglia BV2 cells under oxygen-glucose deprivation (OGD) and CTPtreatment.Results: Our data showed that CTP treatment could improve the functional recovery, as well as suppress the apoptosis, alleviate inflammatory and oxidative response in SCI mice. In addition, CTP was found to be up-regulated miR-142 and the protective effects of CTP on apoptosis, inflammatory and oxidative response may relate to its regulation of HMGB1/TLR4/NF-κB pathway through miR-142.Conclusion: Our findings suggest that CTP may protect the spinal cord from SCI by suppression of apoptosis, oxidative stress and inflammatory response via miR-142/HMGB1/TLR4/NF-κB pathway.

The potential role of heat shock proteins in acute spinal cord injury

2014 ◽  
Vol 23 (7) ◽  
pp. 1480-1490 ◽  
Author(s):  
Yijun Zhou ◽  
Leilei Xu ◽  
Xinghua Song ◽  
Liwen Ding ◽  
Jiangtao Chen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Potential Role ◽  
Acute Spinal Cord Injury ◽  
Cord Injury ◽  
Shock Proteins

scholarly journals Ryanodine Receptor 2 Plays a Critical Role in Spinal Cord Injury via Induction of Oxidative Stress

2016 ◽  
Vol 38 (3) ◽  
pp. 1129-1137 ◽  
Author(s):  
Bo Liao ◽  
Yong Zhang ◽  
Honghui Sun ◽  
Baoan Ma ◽  
Jixian Qian
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Molecular Mechanisms ◽  
Ryanodine Receptors ◽  
Critical Role ◽  
Ros Generation ◽  
Lesion Volume ◽  
Activating Transcription Factor 3 ◽  
Cord Injury

Background/Aims: Spinal cord injury (SCI) is a severe health problem worldwide. Ryanodine receptors (RyRs) are a class of intracellular calcium channels in various excitable tissues such as muscles and nervous tissues. The current study was designed to investigate the possible role of RyR2 upregulation in SCI and to elucidate the possible molecular mechanisms. Methods: Rats were injected with LVshRNAi- RyR2 and then exposed to spinal cord contusion injury. Results: The results showed that knockdown of RyR2 significantly promoted the recovery of structural and functional injury in spinal cord, as evidenced by reduction of lesion volume and increase of Basso, Beattie and Bresnahan (BBB) and combined behavioral score (CBS) scores. Knockdown of RyR2 inhibited the increase of proinflammatory cytokines, including IL-1β and TNFα. Moreover, downregulation of RyR2 increased oxygen consumption rate and decreased the expression of glucose-regulated protein 78 (GRP78), activating transcription factor 3 (ATF3) and ATF6, indicating the improvement of mitochondrial dysfunction and endoplasmic reticulum stress after SCI. Furthermore, silence of RyR2 reduced oxidative stress, as reflected by decrease of TBARS and GSSG content and increase of GSH level. The expression of NADPH oxidase 2 (NOX2), NOX4 and p66shc were increased in SCI rats. Knockdown of RyR2 significantly decreased NOX2 expression, but had no evident effect on NOX4 and p66shc expression. These results indicated NOX2 may be involved in RyR2-induced ROS generation which mediated contusion-induced spinal cord injury. Conclusion: The data provide novel insights into the mechanism of RyR2-mediated injury and the potential therapeutic targets for injury in spinal cord.

Potential Role of Growth Factors in the Management of Spinal Cord Injury

2015 ◽  
Vol 83 (1) ◽  
pp. 120-131 ◽  
Author(s):  
Basem I. Awad ◽  
Margaret A. Carmody ◽  
Michael P. Steinmetz
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Growth Factors ◽  
Potential Role ◽  
Cord Injury

scholarly journals Erratum to: The potential role of heat shock proteins in acute spinal cord injury

2014 ◽  
Vol 23 (7) ◽  
pp. 1582-1582
Author(s):  
Yijun Zhou ◽  
Leilei Xu ◽  
Xinghua Song ◽  
Liwen Ding ◽  
Jiangtao Chen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Potential Role ◽  
Acute Spinal Cord Injury ◽  
Cord Injury ◽  
Shock Proteins
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