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目的研究亚低温对脑损伤后病理学,α-酮戊二酸脱氢酶(α-ketoglutarate dehydrogenase complex,α-KGDHC)活性以及Caspase-3活性的影响。方法雄性SD大鼠50只随机分七组：假手术组(n=5),液压脑损伤常温组(1．8～2．2atm)(n=25),液压脑损伤亚低温组(n=20)。常温组伤后6h,24h,72h,7d检测创伤侧皮层、海马及丘脑线粒体α-KGDHC活性及Caspase-3的活性。伤后15min应用亚低温,30min内脑温降至33℃并维持4h,检测24h及72h酶活性以及Caspase-3的活性。以及亚低温对损伤后24h皮层丘脑及海马CA3区神经病理的影响。结果Fluoro-jade染色显示亚低温显著减少损伤后24h坏死神经元数目(P＜0．05),伤后24h及72h KGDHC酶的活性显著增加(P＜0．05)。伤后24h Caspase-3的活性显著降低(45%)。结论创伤性脑损伤后早期亚低温能够恢复能量代谢酶的活性,抑制神经元凋亡,减轻损伤后神经元的变性。
Objective To investigate the effects of mild hypothermia on the pathology, α-ketoglutarate dehydrogenase complex (α-KGDHC) activity and Caspase-3 activity after brain injury. Methods Fifty male Sprague-Dawley rats were randomly divided into seven groups: sham operation group (n = 5), normal brain injury group (1.8-2.2 atm) (n = 25), mild brain injury brain injury group 20). The mitochondrial α-KGDHC activity and Caspase-3 activity in traumatic cortex, hippocampus and thalamus were detected at 6h, 24h, 72h, 7d after injury at room temperature. Mild hypothermia was applied 15 min after injury, and the temperature was reduced to 33 ℃ in 30 min and maintained for 4 h. The activity of caspase-3 and activity of Caspase-3 were detected 24h and 72h. And the effect of mild hypothermia on the neuropathology of the thalamic and hippocampal CA3 regions in the cortex after 24 h injury. Results Fluoro-jade staining showed that mild hypothermia significantly reduced the number of necrotic neurons 24 hours after injury (P <0.05), and increased the activities of KGDHC enzymes 24h and 72h after injury (P <0.05). Caspase-3 activity was significantly reduced at 24h (45%). Conclusion Early mild hypothermia after traumatic brain injury can restore the activity of energy metabolism enzyme, inhibit neuronal apoptosis and alleviate neuronal degeneration after injury.