scholarly journals The Effect of Safflower Yellow on Spinal Cord Ischemia Reperfusion Injury in Rabbits

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Daiwei Zhou ◽  
Bingbing Liu ◽  
Xiaoshan Xiao ◽  
Peng Dai ◽  
Songmei Ma ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Lipid Peroxidation ◽  
Reperfusion Injury ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Functional Activities ◽  
Hind Limbs ◽  
The One

Safflower yellow (SY) is the safflower extract and is the one of traditional Chinese medicine. The aim of the present work was to investigate the effect of SY on spinal cord ischemia reperfusion injury (SCIRI) in rabbits. The models of spinal cord ischemia reperfusion (SI/R) were constructed, and the degree of the post-ischemic injury was assessed by means of the neurological deficit scores and plasma levels of lipid peroxidation reactioin and neuronal morphologic changes. SCIRI remarkably affected the functional activities of the hind limbs and activated lipid peroxidation reaction. SY could attenuate apoptosis and SCIRI by enhancing Bcl-2 expression and inhibiting Bax and caspase-3 activation.

scholarly journals Nicotinamide Adenine Dinucleotide Protects against Spinal Cord Ischemia Reperfusion Injury-Induced Apoptosis by Blocking Autophagy

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Lei Xie ◽  
Sifei Yu ◽  
Zhenfei Wang ◽  
Kai Yang ◽  
Zhuochao Liu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Reperfusion Injury ◽  
Nicotinamide Adenine Dinucleotide ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Nicotinamide Adenine ◽  
Sprague Dawley ◽  
Induced Apoptosis

The role of autophagy, neuroprotective mechanisms of nicotinamide adenine dinucleotide (NAD+), and their relationship in spinal cord ischemic reperfusion injury (SCIR) was assessed. Forty-eight Sprague-Dawley rats were divided into four groups: sham, ischemia reperfusion (I/R), 10 mg/kg NAD+, and 75 mg/kg NAD+. Western blotting, immunofluorescence, and immunohistochemistry were used to assess autophagy and apoptosis. Basso, Beattie, and Bresnahan (BBB) scores were used to assess neurological function. Expression levels of Beclin-1, Atg12-Atg5, LC3B-II, cleaved caspase 3, and Bax were upregulated in the I/R group and downregulated in the 75 mg/kg NAD+group; p-mTOR, p-AKT, p62, and Bcl-2 were downregulated in the I/R group and upregulated in the 75 mg/kg NAD+group. Numbers of LC3B-positive, caspase 3-positive, Bax-positive, and TUNEL-positive cells were significantly increased in the I/R group and decreased in the 75 mg/kg NAD+group. The mean integrated option density of Bax increased and that of Nissl decreased in the I/R group, and it decreased and increased, respectively, in the 75 mg/kg NAD+group. BBB scores significantly increased in the 75 mg/kg NAD+group relative to the I/R group. No difference was observed between I/R and 10 mg/kg NAD+groups for these indicators. Therefore, excessive and sustained autophagy aggravates SCIR; administration of NAD+alleviates injury.

Exosome miR-23a-3p From Osteoblast Alleviates Spinal Cord Ischemia/Reperfusion Injury by Down-regulating KLF3-activated CCNL2 Transcription

2021 ◽  
Author(s):  
Cheng Wu ◽  
Qinghua Zhu ◽  
Yi Yao ◽  
Zhaoyang Shi ◽  
Chaojie Jin ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Reperfusion Injury ◽  
Regulatory Mechanism ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Neurological Dysfunction ◽  
Aneurysm Surgery ◽  
Aortic Aneurysm Surgery ◽  
Geo Database

Background: Spinal cord ischemia/reperfusion injury (SCIRI) is usually caused by spinal surgery or aortic aneurysm surgery and can eventually lead to paralysis or paraplegia and neurological dysfunction. Exosomes are considered as one of the most promising therapeutic strategies for SCIRI as they can pass the blood-spinal barrier. Previous studies have proved that exosomes secreted by osteocytes have a certain slowing effect on SCIRI. Aim: We aimed to explore the effect of osteoblast secreted exosomes on SCIRI. Methods: Firstly, neurons and osteoblasts were co-cultured under different conditions. GEO database was utilized to detect the expression of miR-23a-3p in osteoblast exosomes. SCIRI cells were treated with exosomes, and the detection was taken to prove whether miR-23a-3p could slow the progression of SCIRI. Downstream gene and the potential regulatory mechanism were explored through database and functional experiments. Results: MiR-23a-3p was highly expressed in exosomes and it slowed down the process of SCIRI. Downstream mRNA KLF3 could bind to miR-23a-3p and was highly expressed in IRI. Moreover, CCNL2 was regulated by KLF3 and was highly expressed in IRI. Rescue experiments verified that miR-23a-3p suppressed the transcription of CCNL2 by targeting KLF3. Conclusion: Exosome miR-23a-3p from osteoblast alleviates SCIRI by down-regulating KLF3-activated CCNL2 transcription.

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