Abstract Spinal cord injury （SCI） remains an unsolved human health challenge. To alleviate the impairments of SCI, we studied the therapeutic effect of nimodipine （an L-type Ca^2＋ channel antagonist） on functiona...Abstract Spinal cord injury （SCI） remains an unsolved human health challenge. To alleviate the impairments of SCI, we studied the therapeutic effect of nimodipine （an L-type Ca^2＋ channel antagonist） on functional recovery from SCI using Nystrom＇s method in a mouse model. Eighty-four mice were divided into three groups： control group in which only vertebral plates were cut off without causing any spinal injuries; SCI; and SCI with nimodipine treatment. We assessed the histopathology, apoptosis detection, cell cycle, mitochondrial transmembrane potential, bcl-2/bax and caspase-3 levels of tissue 8 h, 1 d, 3 d and 4 d after trauma to evaluate rehabilitation. Behavioral performances were also assessed before and after nimodipine treatment. Results from inclined plane tests, motor score assessment and histological observations indicated that mice in the nimodipine-treated group rehabilitated better than those in the SCI group. The ratio of apoptosis, caspase-3 and bax expression in the nimodip- ine-treated group were significantly lower than those in the SCI group. The mitochondrial membrane potential and bcl-2 expression were up-regulated in the nimodipine-treated group. Taken together, our results indicate that the inhibition of calcium flux by nimodipine could reduce apoptosis processes and tissue damage through a mitochondrial pathway after spinal cord trauma [Current Zoology 57 （3）： 340-349, 2011].展开更多
文摘Abstract Spinal cord injury （SCI） remains an unsolved human health challenge. To alleviate the impairments of SCI, we studied the therapeutic effect of nimodipine （an L-type Ca^2＋ channel antagonist） on functional recovery from SCI using Nystrom＇s method in a mouse model. Eighty-four mice were divided into three groups： control group in which only vertebral plates were cut off without causing any spinal injuries; SCI; and SCI with nimodipine treatment. We assessed the histopathology, apoptosis detection, cell cycle, mitochondrial transmembrane potential, bcl-2/bax and caspase-3 levels of tissue 8 h, 1 d, 3 d and 4 d after trauma to evaluate rehabilitation. Behavioral performances were also assessed before and after nimodipine treatment. Results from inclined plane tests, motor score assessment and histological observations indicated that mice in the nimodipine-treated group rehabilitated better than those in the SCI group. The ratio of apoptosis, caspase-3 and bax expression in the nimodip- ine-treated group were significantly lower than those in the SCI group. The mitochondrial membrane potential and bcl-2 expression were up-regulated in the nimodipine-treated group. Taken together, our results indicate that the inhibition of calcium flux by nimodipine could reduce apoptosis processes and tissue damage through a mitochondrial pathway after spinal cord trauma [Current Zoology 57 （3）： 340-349, 2011].
