Effect of hyperbaric oxygen preconditioning on expression of Bcl-2 and Bax after spinal cord injury

doi:10.3969/j.issn.2095-4344.2013.46.007

Abstract

Abstract:

BACKGROUND: Studies have shown that hyperbaric oxygen preconditioning can reduce neuronal apoptosis and improve neurologic dysfunction after spinal cord injury. However, the mechanism of inhibiting apoptosis is still unclear.
OBJECTIVE: To study the effect and significance of hyperbaric oxygen preconditioning on expression of Bcl-2 and Bax protein after spinal cord injury in rats.
METHODS: Sixty-six male adult Sprague-Dawley rats were divided into sham operation group, model group, treatment group at random. Animals in the sham group were six, and animals in the model and treatment groups were 30, respectively. Animals in the treatment group received hyperbaric oxygen preconditioning at 2.5 MPa (100% O₂), once for 1 hour and totally five times within 10 days before establishment of spinal cord injury models. In the sham operation group, only laminectomy was done. In the model group, a spinal cord injury model was prepared using Allen’s method.
RESULTS AND CONCLUSION: The results of immunochemistry indicated that there were few Bcl-2 and Bax-positive cells in the sham operation group; a number of Bcl-2 and Bax-positive cells were visible in the model and treatment groups. Bcl-2 and Bax expressions reached the peak at day 7 and 3, respectively, after injury. After treatment with hyperbaric oxygen preconditioning, Bcl-2 positive cells decreased significantly, while Bax-positive cells decreased significantly (P < 0.05). It indicates that the hyperbaric oxygen preconditioning can increase Bcl-2 expression but decrease Bax expression.

Key words: hyperbaric oxygenation, spinal cord injuries, apoptosis, immunohistochemistry

CLC Number:

R318

Zhang Yu-qiang, Li You, Cao Yang, Dong Ming-yan, Lü Gang. Effect of hyperbaric oxygen preconditioning on expression of Bcl-2 and Bax after spinal cord injury[J]. Chinese Journal of Tissue Engineering Research, 2013, 17(46): 8018-8023.

Figures/Tables 3

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