高压氧通过抑制炎症和神经胶质瘢痕形成来改善损伤脊髓的功能恢复。
Hyperbaric Oxygen Improves Functional Recovery of the Injured Spinal Cord by Inhibiting Inflammation and Glial Scar Formation.
机构信息
From the Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China (YZ, QD, Y. Song, PS, YN, Y. Sun, DL); The Experimental Center, The Second Affiliated Hospital of Soochow University, Suzhou, China (YZ); and Department of Radiology, People's Hospital of Changshan, Quzhou, China (ZP).
出版信息
Am J Phys Med Rehabil. 2019 Oct;98(10):914-920. doi: 10.1097/PHM.0000000000001225.
BACKGROUND
Inflammation and glial scar formation determine the recovery process after spinal cord injury. Hyperbaric oxygen is used as a rehabilitation therapy for various clinical diseases, including spinal cord injury. However, the relationship between hyperbaric oxygen therapy and inflammation or glial scar is not fully understood.
OBJECTIVE
The aim of this study was to investigate the therapeutic effect and molecular mechanism of hyperbaric oxygen on spinal cord injury.
METHODS
A total of 54 developing female Sprague-Dawley rats were randomly divided into sham group, spinal cord injury group, and hyperbaric oxygen group, with 18 rats in each group. The model of spinal cord injury was established using Allen's method. Hyperbaric oxygen therapy was administered once a day until the rats were killed.
RESULTS
The results demonstrated inflammation and glial scar formation are involved in secondary spinal cord injury. After hyperbaric oxygen treatment, there was a notable improvement of the locomotor function in rats. Hyperbaric oxygen reduced the inflammatory reaction and glial scar formation by inhibiting inflammation-related factors iNOS and COX-2 and glial scar-related components GFAP and NG2. This process may be achieved by inhibiting AKT and NF-kB pathways.
CONCLUSIONS
Hyperbaric oxygen effectively promotes the recovery of spinal cord injury by inhibiting inflammation and glial scar formation.
背景
炎症和神经胶质瘢痕形成决定了脊髓损伤后的恢复过程。高压氧作为一种康复治疗方法，用于治疗多种临床疾病，包括脊髓损伤。然而，高压氧治疗与炎症或神经胶质瘢痕之间的关系尚未完全阐明。
目的
本研究旨在探讨高压氧对脊髓损伤的治疗作用及分子机制。
方法
将 54 只雌性发育中的 Sprague-Dawley 大鼠随机分为假手术组、脊髓损伤组和高压氧组，每组 18 只。采用 Allen 法建立脊髓损伤模型。高压氧治疗每天进行一次，直至大鼠处死。
结果
结果表明，炎症和神经胶质瘢痕形成参与了继发性脊髓损伤。高压氧治疗后，大鼠的运动功能明显改善。高压氧通过抑制炎症相关因子 iNOS 和 COX-2 以及神经胶质瘢痕相关成分 GFAP 和 NG2 ，减轻了炎症反应和神经胶质瘢痕形成。这一过程可能是通过抑制 AKT 和 NF-kB 通路实现的。
结论
高压氧通过抑制炎症和神经胶质瘢痕形成，有效地促进了脊髓损伤的恢复。
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