Electroacupuncture pretreatment attenuates spinal cord ischemia-reperfusion injury via inhibition of high-mobility group box 1 production in a LXA4 receptor-dependent manner
Autor: | Xiao-ling Zhu, Xin Chen, Yu-Yuan Min, Yu Wang, Xu Li, Bin-Xiao Su, Wei Wang, Jia Huo, Jian-Ming Pei |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Electroacupuncture medicine.medical_treatment chemical and pharmacologic phenomena Pharmacology HMGB1 Neuroprotection 03 medical and health sciences 0302 clinical medicine medicine Molecular Biology Spinal cord injury biology business.industry General Neuroscience Balloon catheter medicine.disease Spinal cord 030104 developmental biology medicine.anatomical_structure Anesthesia biology.protein Neurology (clinical) business Paraplegia Reperfusion injury 030217 neurology & neurosurgery Developmental Biology |
Zdroj: | Brain Research. 1659:113-120 |
ISSN: | 0006-8993 |
Popis: | Paraplegia caused by spinal cord ischemia is a severe complication following surgeries in the thoracic aneurysm. HMGB1 has been recognized as a key mediator in spinal inflammatory response after spinal cord injury. Electroacupuncture (EA) pretreatment could provide neuroprotection against cerebral ischemic injury through inhibition of HMGB1 release. Therefore, the present study aims to test the hypothesis that EA pretreatment protects against spinal cord ischemia-reperfusion (I/R) injury via inhibition of HMGB1 release. Animals were pre-treated with EA stimulations 30min daily for 4 successive days, followed by 20-min spinal cord ischemia induced by using a balloon catheter placed into the aorta. We found that spinal I/R significantly increased mRNA and cytosolic protein levels of HMGB1 after reperfusion in the spinal cord. The EA-pretreated animals displayed better motor performance after reperfusion along with the decrease of apoptosis, HMGB1, TNF-α and IL-1β expressions in the spinal cord, whereas these effects by EA pretreatment was reversed by rHMGB1 administration. Furthermore, EA pretreatment attenuated the down-regulation of LXA4 receptor (ALX) expression induced by I/R injury, while the decrease of HMGB1 release in EA-pretreated rats was reversed by the combined BOC-2 (an inhibitor of LXA4 receptor) treatment. In conclusion, EA pretreatment may promote spinal I/R injury through the inhibition of HMGB1 release in a LXA4 receptor-dependent manner. Our data may represent a new therapeutic technique for treating spinal cord ischemia-reperfusion injury. |
Databáze: | OpenAIRE |
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