Cryogen spray cooling mitigates inflammation and injury-induced CISD2 decline in rat spinal cord hemisection model

Journal of Integrative Neuroscience

Woon-Man Kung¹  Cheng-Jen Chang²  Muh-Shi Lin³  Tzu-Yung Chen³ 

[1] Department of Exercise and Health Promotion, College of Kinesiology and Health, Chinese Culture University, 111, Taipei, Taiwan;Department of Plastic Surgery, Taipei Medical University Hospital, Taipei Medical University, 110, Taipei, Taiwan;Division of Neurosurgery, Department of Surgery, Kuang Tien General Hospital, 433, Taichung, Taiwan;

关键词: cryogen spray cooling;    hypothermia;    cisd2;    inflammatory responsey;    astrocyte activation;    apoptosis;    neuronal loss;    spinal cord injury;   

DOI  :  10.31083/j.jin.2020.04.255

来源: DOAJ

【 摘 要 】

Therapeutic strategies for traumatic spinal cord injury generally involve rectifying concomitant destruction to the spinal cord from inflammation, mitochondrial dysfunction, and eventual neuronal apoptosis. Elevating the expression of spinal cord injury-attenuated CDGSH iron-sulfur domain-2 has been shown to mitigate the pathologies above. In the current work, hypothermia was induced via continuous cryogen spray cooling in a rat spinal cord hemisection model. Spinal cord injury was shown to elevate the mRNA expression of proinflammatory mediators, including NFκB, iNOS, TNF-α, and regulated upon activation, normal T-cell expressed and secreted as well as lower CDGSH iron-sulfur domain-2 expression. Cryogen spray cooling treatment was shown to attenuate inflammatory reactions and elevate CDGSH iron-sulfur domain-2 expression. Immunohistochemical analysis of the glial fibrillary acidic protein, caspase-3 and NeuN in spinal cord injured rats that underwent cryogen spray cooling treatment revealed notable reductions in injury-induced astrocytic activation, apoptosis, neuronal loss, and decline in CDGSH iron-sulfur domain-2 expression. These results demonstrate the CDGSH iron-sulfur domain-2 preserving effects of cryogen spray cooling, which could contribute to the prevention of astrocytic activation, astrocyte-mediated neuroinflammation, apoptosis, and neuron loss.

【 授权许可】

Unknown