| 刘艳萍
，董强.组织型激肽释放酶通过诱导自噬对缺血性脑卒中发挥保护作用[J].神经损伤功能重建,2023,(知网首发): |
| 组织型激肽释放酶通过诱导自噬对缺血性脑卒中发挥保护作用 |
| Tissue Kallikrein Exerts a Protective Effect on Ischemic Stroke by Inducing Autophagy |
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| DOI： |
| 中文关键词: 组织型激肽释放酶 自噬 永久性大脑中动脉缺血模型 脑梗死体积 |
| 英文关键词: tissue kallikrein autophagy permanent middle cerebral artery occlusion cerebral infarction volume |
| 基金项目:国家自然科学基金
（No. 82101541）；
中央高校基本科研
业 务 费 专 项 资 金
（No. 2042017kf00
95） |
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| 摘要点击次数: 734 |
| 全文下载次数: 816 |
| 中文摘要: |
| 目的：通过在体实验研究组织型激肽释放酶（TK）对缺血性卒中的神经保护作用是否与诱导保护性
自噬有关。方法：成年雄性SD大鼠随机分为假手术组、生理盐水（NS）组、TK组、3-MA组和3-MA+TK组，
每组11只。假手术组和NS组分别于侧脑室注射NS，TK组和3-MA组分别于侧脑室注射TK和自噬抑制剂
3-MA，3-MA+TK组先注射3-MA，30 min 后再注射TK。各组完成侧脑室给药后，采用线栓法建立永久性大
脑中动脉缺血模型（pMCAO）。在缺血后12 h，采用Longa评分法评估各组大鼠的神经功能。完成神经损
伤评分后，TTC染色检测各组大鼠脑梗死体积，免疫印迹实验检测各组自噬相关蛋白LC3和p62的表达水
平。结果：NS组大鼠缺血侧脑皮质LC3-Ⅱ较假手术组表达升高，p62水平降低（均P＜0.01）。与NS组相比，
TK组缺血侧脑皮质LC3-Ⅱ表达增高，p62水平降低（均P＜0.01），大鼠神经功能损伤较轻、脑梗死体积明显
缩小（均P＜0.01）；与TK组比较，3-MA组缺血脑皮质LC3-Ⅱ的表达降低和p62的水平水平较高，大鼠神经
功能损伤较重、脑梗死体积较大（均P＜0.01）；与TK组相比，3-MA+TK组大鼠神经损伤评分增加、脑梗死体
积明显增加（均P＜0.01）。结论：TK对缺血性卒中大鼠具有神经保护作用，其机制与诱导自噬发生有关。 |
| 英文摘要: |
| To investigate whether the neuroprotective effect of tissue kallikrein (TK) on ischemic
stroke is related to the induction of protective autophagy by in vivo experiments. Methods: Adult male SD rats
were randomly divided into sham surgery group, normal saline (NS) group, TK group, 3-MA group and 3-MA+
TK group, with 11 rats in each group. Rats in the sham group and the NS group were injected NS in the lateral
ventricle, rats in the TK group and in the 3-MA group were injected TK and autophagy inhibitor 3-MA in the lateral ventricle respectively, and rats in the 3-MA+TK group were injected with 3-MA and then injected with TK
30 min later. Permanent middle cerebral artery occlusion (pMCAO) model was established by thread embolism
after the lateral ventricle administration was completed in each group. At 12 h post-ischemia, the neurological
function of rats in each group was assessed by Longa score. After the completion of nerve injury assessment, the
cerebral infarction volume of rats in each group was detected by TTC staining, and the expression levels of autophagy related proteins LC3 and p62 were detected by western blotting. Results: The expression of LC3-Ⅱ in
ischemic cortex of NS group was higher than that in sham group, and the expression of p62 was lower (both P<
0.01). Compared with the NS group, the expression of LC3-II in the ischemic side cerebral cortex of the TK
group was increased, the expression of p62 decreased, the neurological damage of rats was milder, and the volume of cerebral infarction was significantly reduced (all P<0.01). Compared with the TK group, the expression
of ischemic cerebral cortex LC3-II and the expression level of p62 were higher in the 3-MA group, and the rats
had more severe neurological damage and larger cerebral infarction volume (all P<0.01). Compared with the TK
group, the score of nerve damage and the volume of cerebral infarction increased significantly in the 3-MA+TK
group (all P<0.01). Conclusion: TK has a neuroprotective effect on ischemic stroke rats, and its mechanism is
related to the induction of autophagy genesis. |
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