关键词: 神经再生, 脊髓损伤, 线粒体, 融合, 分裂, 氧化损伤, 生物能量, 线粒体通透性, 细胞色素C, Caspase-3, 凋亡, 国家自然科学基金

Abstract:

Changes in mitochondrial morphology and function play an important role in secondary damage after acute spinal cord injury. We recorded
the time representation of mitochondrial morphology and function in rats with acute spinal cord injury. Results showed that mitochondria had an irregular shape, and increased in size. Mitochondrial cristae were disordered and mitochondrial membrane rupture was visible at 2–24 hours after injury. Fusion protein mitofusin 1 expression gradually increased, peaked at 8 hours after injury, and then decreased to its lowest level at 24 hours. Expression of dynamin-related protein 1, amitochondrial fission protein, showed the opposite kinetics. At 2–24 hours after acute spinal cord injury, malondialdehyde content, cytochrome c levels and caspase-3 expression were increased,but glutathione content, adenosine triphosphate content, Na+-K+-ATPase activity and mitochondrial membrane potential were gradually reduced. Furthermore, mitochondrial morphology altered during the acute stage of spinal cord injury. Fusion was important within the first 8 hours, but fission played a key role at 24 hours. Oxidative stress was inhibited, biological productivity was diminished, and mitochondrial membrane potential and permeability were reduced in the acute stage of injury. In summary, mitochondrial apoptosis is activated when the time of spinal cord injury is prolonged.

Key words: nerve regeneration, spinal cord injury, mitochondria, fusion, fission, oxidative damage, bioenergy, mitochondrial permeability, cytochrome c, Caspase-3, apoptosis, NSFC, neural regeneration