P39 Inhaled hydrogen sulfide can prevent delayed neuronal death after spinal cord ischemia in mice

Nitric Oxide ◽  
2014 ◽  
Vol 39 ◽  
pp. S28
Author(s):  
Manabu Kakinohana ◽  
Kotaro Kida ◽  
Fumito Ichinose
2004 ◽  
Vol 47 (3) ◽  
pp. 209-211
Author(s):  
Eva Mechírová ◽  
Iveta Domoráková ◽  
Marianna Feriková

Using ubiquitin immunohistochemistry and impregnative Nauta method we demonstrated that ubiquitin positivity and Nauta positivity in the neurons affected with ischemic injury in the lumbosacral spinal cord of rabbits and dogs may be of the same origin. Increased number of ubiquitin-positive aggregates was found in the cytoplasm of neurons in the intermediate zone and lamina IX of ventral horns of spinal cord in rabbits after 30 min of ischemia followed by 24 h lasting reperfusion. Nauta-positive, flocculent, intracytoplasmic, dark clusters appeared in the same localization in the canine lumbosacral spinal cord neurons after 30 min of ischemia and 24 h of reperfusion. Ubiquitin aggregates and Nauta-positive dark clusters in the injured spinal cord neurons could be the first light microscopic signs of slow neuronal death following spinal cord ischemia and reperfusion.


2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Lei Xie ◽  
Sifei Yu ◽  
Kai Yang ◽  
Changwei Li ◽  
Yu Liang

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.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S452-S452
Author(s):  
Noritaka Murakami ◽  
Masahiro Sakurai ◽  
Takashi Horinouchi ◽  
Jun Ito ◽  
Shin Kurosawa ◽  
...  

2010 ◽  
Vol 58 (S 01) ◽  
Author(s):  
B Zipfel ◽  
S Buz ◽  
R Hammerschmidt ◽  
V Düsterhöft ◽  
R Hetzer

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