| Literature DB >> 25550916 |
Ying Long1, Fang Liang2, Chunjin Gao2, Zhuo Li2, Jing Yang2.
Abstract
Hyperbaric oxygen therapy (HBOT) protects brain tissue from inflammatory injury by suppressing mitochondrial apoptotic pathways. However, its neuroprotective mechanism via anti-apoptosis in spinal cord injury (SCI) is still unclear. In our study, Male Sprague-Dawley rats were randomly divided into three groups: sham-operated (SH), SCI model, and SCI + HBOT. Rats in each group were randomly divided into four sub-groups in a time-dependent manner (1 day, 3 days, 7 days and 14 days after surgery). Expression of adaptor molecule apoptosis-associated speck-like protein (ASC) and caspase-3 was evaluated at the indicated time after injury. Our data showed that HBOT downregulated expression of ASC in SCI rats at the mRNA and protein levels. HBOT mitigated caspase-3 release in injured spinal cord tissue. We conclude that HBOT prevents inflammation apoptosis after SCI, likely through suppression of ASC and caspase-3.Entities:
Keywords: Hyperbaric oxygen therapy; apoptosis-associated speck-like protein; caspase-3; spinal cord injury
Year: 2014 PMID: 25550916 PMCID: PMC4276174
Source DB: PubMed Journal: Int J Clin Exp Med ISSN: 1940-5901