Recovery from Traumatic Brain Injury Following Treatment with Δ9-Tetrahydrocannabinol Is Associated with Increased Expression of Granulocyte-Colony Stimulating Factor and Other Neurotrophic Factors.
Recovery from Traumatic Brain Injury Following Treatment with Δ9-Tetrahydrocannabinol Is Associated with Increased Expression of Granulocyte-Colony Stimulating Factor and Other Neurotrophic Factors.
复制标题
α9-四氢大麻酚治疗后脑外伤的恢复与粒细胞集落刺激因子和其他神经营养因子表达的增加有关。
DOI：
10.1089/can.2020.0119
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发表时间：
2022
影响因子：
3.8
通讯作者：
Sanchez-Ramos,Juan
中科院分区：
文献类型：
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作者：
Song,Shijie;Kong,Xiaoyuan;Wang,Bangmei;Sanchez-Ramos,Juan
前言：造血细胞因子粒细胞集落刺激因子(G-CSF)不仅能刺激外周血白细胞系的干/祖细胞增殖，还被认为是参与脑自我修复过程的神经营养因子。G-CSF的应用已被证明可以促进创伤性脑损伤(TBI)实验模型的恢复，并调节内源性大麻素系统(ECS)的成分。相反，Δ9-四氢大麻酚(Δ9THC)对正常小鼠外周血中G-Csf水平有促进作用。结论：给予植物大麻素Δ9THC可通过上调脑区G-Csf和其他神经营养因子(脑源性神经营养因子和胶质源性神经营养因子)，促进受控皮质撞击后的脑修复。材料和方法：C57BL/6J小鼠接受C57BL/6J小鼠CCI，THC 3 mg/kg，连续3天。在基线和CCI后3、7和14天记录旋转棒的运动功能。分别于第7天和第14天处死小鼠。结果：Δ9THC治疗组小鼠在旋转棒上行走的时间明显长于赋形剂组，在伤后2周恢复到正常旋转棒运动水平。结论：给予植物大麻素Δ9THC可显著促进脑损伤的恢复，并与脑G-CSF、脑源性神经营养因子和胶质细胞源性神经营养因子的上调有关。
Introduction:The hematopoietic cytokine granulocyte-colony stimulating factor (G-CSF) is well known to stimulate proliferation of blood stem/progenitor cells of the leukocyte lineage, but is also recognized as a neurotrophic factor involved in brain self-repair processes. G-CSF administration has been shown to promote recovery from experimental models of traumatic brain injury (TBI) and to modulate components of the endocannabinoid system (eCS). Conversely, Δ9-tetrahydrocannabinol (Δ9THC) treatment of normal mice has been shown to increase blood levels of G-CSF in the periphery.Hypothesis:Administration of the phytocannabinoidΔ9THC will enhance brain repair following controlled cortical impact (CCI) by upregulating G-CSF and other neurotrophic factors (brain-derived neurotrophic factor [BDNF] and glial-derived neurotrophic factor [GDNF]) in brain regions.Materials and Methods:C57BL/6J mice underwent CCI and were treated for 3 days with THC 3 mg/kg intraperitoneally. Motor function on a rotarod was recorded at baseline and 3, 7, and 14 days after CCI. Groups of mice were euthanized at 7 and 14 days. G-CSF, BDNF, and GDNF expression were measured at 7 and 14 days in cerebral cortex, striatum, and hippocampus on the side of the trauma.Results:Δ9THC-treated mice ran on the rotarod longer than vehicle-treated mice and recovered to normal rotarod performance levels at 2 weeks. These mice, compared to vehicle-treated animals, exhibited significant upregulation of G-CSF as well as BDNF and GDNF in cerebral cortex, striatum, and hippocampus.Conclusion:Administration of the phytocannabinoidΔ9THC promotes significant recovery from TBI and is associated with upregulation of brain G-CSF, BDNF, and GDNF, neurotrophic factors previously shown to mediate brain self-repair following TBI and stroke.