IMR Press / JIN / Volume 19 / Issue 4 / DOI: 10.31083/j.jin.2020.04.255
Open Access Original Research
Cryogen spray cooling mitigates inflammation and injury-induced CISD2 decline in rat spinal cord hemisection model
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1 Department of Exercise and Health Promotion, College of Kinesiology and Health, Chinese Culture University, 111, Taipei, Taiwan
2 Department of Plastic Surgery, Taipei Medical University Hospital, Taipei Medical University, 110, Taipei, Taiwan
3 Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, 110, Taipei, Taiwan
4 Graduate Institute of Biomedical Optomechatronics, College of Biomedical Engineering, Taipei Medical University, 110, Taipei, Taiwan
5 Department of Plastic and Reconstructive Surgery, Chang Gung Memorial Hospital, Chang Gung University, 333, Taipei, Taiwan
6 Division of Neurosurgery, Department of Surgery, Kuang Tien General Hospital, 433, Taichung, Taiwan
7 Department of Biotechnology and Animal Science, College of Bioresources, National Ilan University, 260, Yilan, Taiwan
8 Department of Biotechnology, College of Medical and Health Care, Hung Kuang University, 433, Taichung, Taiwan
9 Department of Health Business Administration, College of Medical and Health Care, Hung Kuang University, 433, Taichung, Taiwan
*Correspondence: (Muh-Shi Lin)
J. Integr. Neurosci. 2020, 19(4), 619–628;
Submitted: 24 August 2020 | Revised: 4 December 2020 | Accepted: 4 December 2020 | Published: 30 December 2020
Copyright: © 2020 Kung et al. Published by IMR Press.
This is an open access article under the CC BY 4.0 license (

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 NF κ B, 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.

Cryogen spray cooling
inflammatory response
astrocyte activation
neuronal loss
spinal cord injury
Fig. 1.
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