| Background: Spinal cord injury (SCI) could lead to the loss of sensory andmotor function below the injury level which turns out to be a tough problem in clinical treatment. Recent study presumes that there are two mechanisms could bring about poison effect to the spinal cord. One mechanism is called primary injury including the mechanical pressure, bleeding, electrolyte efflux from the injured cells. The other one is called secondary injury including edema, inflammatory reaction, ischemia, growth factor, cytokines, reperfusion, calcium overload, apoptosis, microcirculation disturbance, lipid peroxidation, and the abmormal change of the peroxidized groups. Secondary changes could turn the SCI from reversible injury to irreversable injury which would result in the neurons apoptosis and finally long-term loss of the neurological function.Study shows that majority of the neurons die of the cell apoptosis secondary to SCI. Apoptosis is regulated by certain genes such as the Bcl-2 family, P53 gene and Caspase family et al. Among them, Bcl-2 family is the important gene that regulates the programmed cell death. It includes two categories, that is, promote survival family and promote apoptosis family. Earlier and more study were done about Bcl-2 in the promote survival family and the study suggested that it had the inhibitory action on both apoptosis and necrosis. Bcl-2 regulates the cells through multiple pathways. It could adjust the redox state of the cells and inhibits the production of the active oxygen during the death of the neurons through the anti-oxidative pathway. The expression of Bcl-2 facilitates the inhibitory of the neurotoxicity of the glumatic acid, relieves the calcium overload and free radicals accumulation in the neurons.
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