| 姜黄素通过PI3K/AKT信号通路激活细胞自噬对大鼠颅脑损伤的神经保护作用 |
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| 引用本文： | 杨伟科,孙林林,李小亮.姜黄素通过PI3K/AKT信号通路激活细胞自噬对大鼠颅脑损伤的神经保护作用[J].中国临床神经外科杂志,2020,0(9):613-617. |
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| 作者姓名： | 杨伟科 孙林林 李小亮 |
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| 作者单位： | 450000，郑州市第七人民医院神经外科（杨伟科、孙林林）；063000 河北唐山，华北理工大学附属医院神经外科（李小亮） |
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| 摘 要： | 目的 探讨姜黄素对颅脑损伤（TBI大鼠）的神经保护作用及其机制。方法 48只成年雄性SD大鼠随机分成假手术组、TBI组、溶媒组、姜黄素组，每组12只。采用重物撞击法制作控制皮质冲击伤模型。造模后，姜黄素组腹腔注射姜黄素（60 mg/kg），溶媒组腹腔注射姜黄素溶媒磷酸缓冲盐溶液；姜黄素干预72 h采用改良神经功能损伤量表（mNSS）评分评估神经功能；每组取6只大鼠采用Nissl染色评估损伤面积，采用TUNEL染色评估细胞凋亡率；另取6只大鼠免疫印迹法检测PI3K/AKT信号通路以及细胞自噬相关蛋白（LC3、Beclin-1、P62蛋白）表达水平。结果 与假手术组比较，TBI组和溶媒组mNSS评分显著增加（P<0.05），损伤面积和神经元凋亡率均明显增加（P<0.05），LC3、Beclin-1表达水平明显增高（P<0.05），P62表达水平明显降低（P<0.05），而PI3K和AKT蛋白表达水平无明显变化（P>0.05）；TBI组和溶媒组均无统计学差异（P>0.05）。与溶媒组相比，姜黄素组mNSS评分明显下降（P<0.05），损伤面积和神经元凋亡率显著降低（P<0.05），磷酸化PI3K/AKT水平明显增高（P<0.05），LC3、Beclin-1表达水平明显增高（P<0.05），P62表达水平明显降低（P<0.05）。结论 姜黄素对TBI大鼠具有显著神经保护作用，机制可能是通过PI3K/AKT信号通路激活自噬
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| 关 键 词： | 颅脑损伤 姜黄素 PI3K/AKT 细胞自噬 大鼠 |
Neuroprotective effect of curcumin on traumatic brain injury by activating autophagy via PI3K/AKT signaling pathway in adult rats |
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| YANG Wei-ke,SUN Lin-lin,LI Xiao-liang..Neuroprotective effect of curcumin on traumatic brain injury by activating autophagy via PI3K/AKT signaling pathway in adult rats[J].Chinese Journal of Clinical Neurosurgery,2020,0(9):613-617. |
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| Authors: | YANG Wei-ke SUN Lin-lin LI Xiao-liang |
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| Affiliation: | 1. Department of Neurosurgery, Zhengzhou No. 7 People's Hospital, Zhengzhou 450000, China; 2. Department of Neurosurgery, North China University of Science and Technology Affiliated Hospital, Tangshan 063000, China |
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| Abstract: | Objective To explore the neuroprotective effect of curcumin on rats after traumatic brain injury (TBI). Methods Forty-eight male SD rats were randomly divided into sham operation group, TBI group, viechle group and curcumin group, 12 rats in each group. A heavy object impact method was used to establish the model of controlled cortical impact injury. After injury, the curcumin group was intraperitoneally injected with curcumin (60 mg/kg), and the vehicle group was intraperitoneally injected with curcumin solvent phosphate buffered saline solution. Seventy-two hours after curcumin treatment, the neurological function was evaluated using the modified neurological impairment scale (mNSS). Six rats in each group were used to evaluate the damage area by Nissl staining and the apoptosis rate by TUNEL staining after the evaluation of neurological function. Six rats in each group were used to detect PI3K/AKT signaling pathway and the expression level of autophagy-related proteins (LC3, Beclin-1, P62 protein) by western blotting. Results Compared with the sham operation group, the mNSS score, the injury area, the neuronal apoptosis rate and the expression levels of LC3 and Beclin-1 were significantly increased (P<0.05), the expression level of P62 was significantly reduced (P<0.05), and the expression levels of PI3K and AKT protein did not significantly change (P>0.05) in TBI and vehicle groups. There was no statistical difference between the TBI and vehicle groups (P<0.05). Compared with the vehicle group, the mNSS score, the damage area and the neuronal apoptosis rate were significantly reduced (P<0.05), the phosphorylated PI3K/AKT level was significantly increased (P<0.05), the LC3 and Beclin-1 expression levels were significantly increased (P<0.05), and the expression level of P62 was significantly decreased (P<0.05) in curcumin group. Conclusion The curcumin has neuroprotective effect on rats after TBI by activating autophagy via PI3K/AKT signaling pathway |
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| Keywords: | Traumatic brain injury Curcumin PI3K/AKT Autophagy Rat |
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