Abstract
Acute traumatic spinal cord injury (tSCI) results in a lifetime of paralysis associated with a host of medical complications. The developing secondary complications of tSCI may result in further chronic neurodegenerative diseases. Sevoflurane preconditioning (SF-PreCon) has shown guaranteed protective effects in myocardial or cerebral ischemic/reperfusion injury. However, the role of SF-PreCon in tSCI still remains to be elucidated. Here, we found that SF-PreCon ameliorated the developing secondary complications through reducing the apoptosis rate and the secretion of inflammatory cytokines in injured spinal cord tissues, and therefore enhancing the recovery after tSCI. Notably, we demonstrated that SF-PreCon ameliorates tSCI through inhibiting Cycloxygenase-2 (COX-2). Importantly, we verified that SF-PreCon inhibits the expression of COX-2 and reduces the apoptosis rate after tSCI via the induction of Caveolin-3 (Cav-3). Taken together, our results suggest that SF-PreCon ameliorates tSCI via Cav-3-dependent COX-2 inhibition and provide an economical and practical method against the secondary injury after tSCI.
Highlights
Traumatic spinal cord injury occurs from external impacts such as motor vehicle collisions, sports accidents, falls, or violence and has two phases: a primary injury phases and a secondary injury phases
Our results suggest that SF-PreCon ameliorates traumatic spinal cord injury (tSCI) via Cav-3-dependent COX-2 inhibition and provide an economical and practical method against the secondary injury after tSCI
The SF-PreCon group with tSCI: five adult female SD rats were subjected to tSCI after SF-PreCon, within which rats were exposed to 3 cycles of 10-minute exposure to 0.5 minimum alveolar concentration (MAC) sevoflurane interspersed with 15 minutes of washout (Figure 1A)
Summary
Traumatic spinal cord injury (tSCI) occurs from external impacts such as motor vehicle collisions, sports accidents, falls, or violence and has two phases: a primary injury phases and a secondary injury phases. After the primary spinal cord injury, the injured area was infiltrated with neutrophils, and the secretion of cytokines attracts other inflammatory cells, that would aggravate the local injury, termed secondary injury [1]. Secondary injury is the main obstacle for the recovery of tSCI, which is induced by the change of the niche microenvironment, that leading to a further tissue ischemia, hypoxia, inflammation aggravate, and forming a vicious circle. The secondary injury may result in further chronic neurodegenerative diseases [2]. The efficient therapies against the secondary injury of tSCI remain urgently to be explored
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