scholarly journals Hydrogen Sulfide Inhibits Autophagic Neuronal Cell Death by Reducing Oxidative Stress in Spinal Cord Ischemia Reperfusion Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Lei Xie ◽  
Sifei Yu ◽  
Kai Yang ◽  
Changwei Li ◽  
Yu Liang
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Cell Death ◽  
Hydrogen Sulfide ◽  
Motor Function ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Autophagic Cell Death

Autophagy is upregulated in spinal cord ischemia reperfusion (SCIR) injury; however, its expression mechanism is largely unknown; moreover, whether autophagy plays a neuroprotective or neurodegenerative role in SCIR injury remains controversial. To explore these issues, we created an SCIR injury rat model via aortic arch occlusion. Compared with normal controls, autophagic cell death was upregulated in neurons after SCIR injury. We found that autophagy promoted neuronal cell death during SCIR, shown by a significant number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling- (TUNEL-) positive cells colabeled with the autophagy marker microtubule-associated protein 1 light chain 3, while the autophagy inhibitor 3-methyladenine reduced the number of TUNEL-positive cells and restored neurological and motor function. Additionally, we showed that oxidative stress was the main trigger of autophagic neuronal cell death after SCIR injury and N-acetylcysteine inhibited autophagic cell death and restored neurological and motor function in SCIR injury. Finally, we found that hydrogen sulfide (H2S) inhibited autophagic cell death significantly by reducing oxidative stress in SCIR injury via the AKT-the mammalian target of rapamycin (mTOR) pathway. These findings reveal that oxidative stress induces autophagic cell death and that H2S plays a neuroprotective role by reducing oxidative stress in SCIR.

scholarly journals MLN4924 Exerts a Neuroprotective Effect against Oxidative Stress via Sirt1 in Spinal Cord Ischemia-Reperfusion Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Sifei Yu ◽  
Lei Xie ◽  
Zhuochao Liu ◽  
Changwei Li ◽  
Yu Liang
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Sirtuin 1

Oxidative stress is a leading contributor to spinal cord ischemia-reperfusion (SCIR) injury. Recently, MLN4924, a potent and selective inhibitor of the NEDD8-activating enzyme, was shown to exert a neuroprotective effect against oxidative stress in vitro. However, it is unknown whether MLN4924 plays a protective role against SCIR injury. In the present study, we found that MLN4924 treatment significantly attenuated oxidative stress and neuronal cell death induced by H2O2 in SH-SY-5Y neural cells and during rat SCIR injury. Furthermore, MLN4924 administration restored neurological and motor functions in rats with SCIR injury. Mechanistically, we found that MLN4924 protects against H2O2- and SCIR injury-induced neurodegeneration by regulating sirtuin 1 (Sirt1) expression. Collectively, these findings demonstrate the neuroprotective role of MLN4924 against oxidative stress in SCIR injury via Sirt1.

scholarly journals Fas Receptor and Neuronal Cell Death after Spinal Cord Ischemia

2000 ◽  
Vol 20 (18) ◽  
pp. 6879-6887 ◽  
Author(s):  
Kohji Matsushita ◽  
Yongqin Wu ◽  
Jianhua Qiu ◽  
Loic Lang-Lazdunski ◽  
Lorenz Hirt ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Spinal Cord Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Fas Receptor

scholarly journals Linolenic acid prevents neuronal cell death and paraplegia after transient spinal cord ischemia in rats

2003 ◽  
Vol 38 (3) ◽  
pp. 564-575 ◽  
Author(s):  
Loïc Lang-Lazdunski ◽  
Nicolas Blondeau ◽  
Gisèle Jarretou ◽  
Michel Lazdunski ◽  
Catherine Heurteaux
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Linolenic Acid ◽  
Spinal Cord Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Insulin-like growth factor 1 prevents neuronal cell death and paraplegia in the rabbit model of spinal cord ischemia

2001 ◽  
Vol 122 (1) ◽  
pp. 136-143 ◽  
Author(s):  
Yoshihisa Nakao ◽  
Hajime Otani ◽  
Tadashi Yamamura ◽  
Reiji Hattori ◽  
Motohiko Osako ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Growth Factor ◽  
Spinal Cord Ischemia ◽  
Neuronal Cell Death ◽  
Rabbit Model ◽  
Neuronal Cell ◽  
Insulin Like Growth Factor

scholarly journals miR-380-5p facilitates NRF2 and attenuates cerebral ischemia/reperfusion injury-induced neuronal cell death by directly targeting BACH1

2021 ◽  
Vol 12 (1) ◽  
pp. 210-217
Author(s):  
Yibiao Wang ◽  
Min Xu
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Luciferase Assay ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion

Abstract Background This study aimed to explore the role of miR-380-5p in cerebral ischemia/reperfusion (CIR) injury-induced neuronal cell death and the potential signaling pathway involved. Methodology Human neuroblastoma cell line SH-SY5Y cells were used in this study. Oxygen and glucose deprivation/reperfusion (OGD/R) model was used to mimic ischemia/reperfusion injury. CCK-8 assay and flow cytometry were used to examine cell survival. Quantitative real time PCR (RT-qPCR) assay and Western blotting were used to measure the change of RNA and protein expression, respectively. TargetScan and Luciferase assay was used to confirm the target of miR-380-5p. Malondialdehyde (MDA) superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) were measured using commercial kits. Results miR-380-5p was downregulated in SH-SY5Y cells after OGD/R. Cell viability was increased by miR-380-5p, while cell apoptosis was reduced by miR-380-5p mimics. MDA was reduced by miR-380-5p mimics, while SOD and GSHPx were increased by miR-380-5p. Results of TargetScan and luciferase assay have showed that BACH1 is the direct target of miR-380-5p. Expression of NRF2 was upregulated after OGD/R, but was not affected by miR-380-5p. mRNA expression of HO-1 and NQO1 and ARE activity were increased by miR-380-5p. Overexpression of BACH1 reversed the antioxidant and neuroprotective effects of miR-380-5p. Conclusion miR-380-5p inhibited cell death induced by CIR injury through target BACH1 which also facilitated the activation of NRF2, indicating the antioxidant and neuroprotective effects of miR-380-5p.

A-fiber sensory input induces neuronal cell death in the dorsal horn of the adult rat spinal cord

2001 ◽  
Vol 435 (3) ◽  
pp. 276-282 ◽  
Author(s):  
Richard E. Coggeshall ◽  
Helena A. Lekan ◽  
Fletcher A. White ◽  
Clifford J. Woolf
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Dorsal Horn ◽  
Sensory Input ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Spinal Cord ◽  
Adult Rat ◽  
Adult Rat Spinal Cord

scholarly journals Induction of the Nrf2 Pathway by Sulforaphane Is Neuroprotective in a Rat Temporal Lobe Epilepsy Model

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1702
Author(s):  
Sereen Sandouka ◽  
Tawfeeq Shekh-Ahmad
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Antioxidant Capacity ◽  
Temporal Lobe ◽  
Epileptiform Activity ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
The Brain

Epilepsy is a chronic disease of the brain that affects over 65 million people worldwide. Acquired epilepsy is initiated by neurological insults, such as status epilepticus, which can result in the generation of ROS and induction of oxidative stress. Suppressing oxidative stress by upregulation of the transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown to be an effective strategy to increase endogenous antioxidant defences, including in brain diseases, and can ameliorate neuronal damage and seizure occurrence in epilepsy. Here, we aim to test the neuroprotective potential of a naturally occurring Nrf2 activator sulforaphane, in in vitro epileptiform activity model and a temporal lobe epilepsy rat model. Sulforaphane significantly decreased ROS generation during epileptiform activity, restored glutathione levels, and prevented seizure-like activity-induced neuronal cell death. When given to rats after 2 h of kainic acid-induced status epilepticus, sulforaphane significantly increased the expression of Nrf2 and related antioxidant genes, improved oxidative stress markers, and increased the total antioxidant capacity in both the plasma and hippocampus. In addition, sulforaphane significantly decreased status epilepticus-induced neuronal cell death. Our results demonstrate that Nrf2 activation following an insult to the brain exerts a neuroprotective effect by reducing neuronal death, increasing the antioxidant capacity, and thus may also modify epilepsy development.

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