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| The effect of hyperbaric oxygen therapy and Notch signal channel blocker on proliferation and differentiation of neural stem cells in rats with traumatic brain injury |
| YANG Yong-kai1 ZHANG Fan1▲ WEI Hao1 ZHOU Xiao-hui1 CHEN Chun-mei2 WANG Chun-hua2 TU Xian-kun2 |
1.Department of Neurosurgery,the First Hospital of Fuzhou City Affiliated to Fujian Medical University,Fujian Province,Fuzhou 350009,China;
2.Department of Neurosurgery,Fujian Medical University Union Hospital,Fujian Province,Fuzhou 350001,China |
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Abstract Objective To observe the effects of hyperbaric oxygen therapy and DAPT on the proliferation and differentiation of endogenous neural stem cells after traumatic brain injury.Methods 100 adult Wistar rats were randomly divided into sham-operation group,traumatic brain injury group,DAPT group,hyperbaric oxygen therapy group and DMSO group.Animal models of craniocerebral trauma were made using the improved free-fall method in the rats.The proliferation and differentiation of neural stem cells of the DG brain tissue was detected by BrdU labeling fluorescence immunocytochemistry at the 7,14,21 d and 28 d after injury.Results The BrdU and nestin positive cells of the traumatic brain injury group,DAPT group and hyperbaric oxygen therapy group began to increase from the 7 d(14.2±1.3,11.4±1.7,22.3±1.5)to the 14 d after injury(9.6±0.7,6.9±2.1,13.8±1.4).Compared with the 14 d,the BrdU and nestin positive cells significantly increased 7 d after injury(P＜0.05).Compared with the traumatic brain injury group,the BrdU and nestin positive cells significantly decreased in the DAPT group 7 d and 14 d after injury(P＜0.05).Compared with the traumatic brain injury group,the BrdU and nestin positive cells significantly increased in the hyperbaric oxygen therapy group 7 d and 14 d after injury (P＜0.05).Conclusion Hyperbaric oxygen therapy can enhance the proliferation and differentiation of endogenous neural stem cells after traumatic brain injury.Notch signal channel blocker can restrain the proliferation and differentiation of endogenous neural stem cells after traumatic brain injury.
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