| 引用本文: | 穆秉桃,郭敏芳,于婧文,张慧宇*.雷公藤甲素通过调节cAMP/PKA/BDNF信号通路促进脑缺血再灌注损伤神经元可塑性[J].中国现代应用药学,2024,41(7):911-916. |
| MU Bingtao,GUO Minfang,YU Jingwen,ZHANG Huiyu*.Triptolide Promote Neuronal Plasticity with Cerebral Ischemia-reperfusion Injury by Regulating the cAMP/PKA/BDNF Signaling Pathway[J].Chin J Mod Appl Pharm(中国现代应用药学),2024,41(7):911-916. |
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| 摘要: |
| 目的 研究雷公藤甲素(triptolide，TP)对脑缺血再灌注(ischemia-reperfution，I/R)损伤大鼠的疗效评价及其发挥效能的机制。方法 大脑中动脉线栓法手术复制大鼠脑I/R损伤模型，治疗组给予TP(0.1，0.2 mg·kg?1)，同时设假手术组。Longa评分法测评鼠神经功能，尼氏染色呈现大鼠缺血侧脑组织神经元形态，免疫荧光法检测缺血侧脑组织中MAP2和Syn的表达水平。Western blotting 法检测cAMP、PKA、BDNF、Syn、PSD-95的表达水平。结果 与模型组比较，TP治疗组神经学评分明显下降(P<0.01或P<0.001)，对损伤神经元有保护作用，且TP治疗组cAMP、PKA、BDNF、PSD-95、Syn的表达均显著上调。结论 TP治疗能显著改善I/R损伤，其机制可能与激活cAMP/PKA/BDNF信号通路有关。 |
| 关键词: 雷公藤甲素 缺血再灌注 突触可塑性 环磷酸腺苷 蛋白激酶A 脑源性神经营养因子 |
| DOI：10.13748/j.cnki.issn1007-7693.20221977 |
| 分类号:R285.5 |
| 基金项目:山西省基础研究计划项目(20210302123478，20210302123476，20210302123337) |
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| Triptolide Promote Neuronal Plasticity with Cerebral Ischemia-reperfusion Injury by Regulating the cAMP/PKA/BDNF Signaling Pathway |
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MU Bingtao1, GUO Minfang1, YU Jingwen1, ZHANG Huiyu*2
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1.Shanxi Datong University, Medical College, Datong 037009, China;2.Shanxi Datong University, College of Traditional Chinese Medicine Health Service, Datong 037009, China
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| Abstract: |
| OBJECTIVE To study the efficacy evaluation of triptolide(TP) in rats with cerebral ischemia-reperfusion(I/R) injury and its mechanism. METHODS Rat brain I/R injury model was copied by middle cerebral artery wire embolism surgery, and TP (0.1, 0.2 mg·kg?1) was given to the treatment group, and set the sham surgery group. The Longa score method was used to measure the neural function of rats, and Niselferi staining was used to show the morphology of neurons in the ischemic side brain tissue of rats, immunofluorescence was used to detect the expression levels of MAP2 and Syn in ischemic lateral brain tissue. The expression levels of cAMP, PKA, BDNF, Syn and PSD-95 were detected by Western blotting. RESULTS Compared with the model group, the neurological scores of TP treatment group decreased significantly(P<0.01 or P<0.001), it had a protective effect on damaged neurons. Compared with the model group, cAMP, PKA, BDNF, Syn and PSD-95 in TP treatment group were significantly up-regulated. CONCLUSION TP treatment can significantly improve I/R injury, and the mechanism may be related to the activation of the cAMP/PKA/BDNF signaling pathway. |
| Key words: triptolide ischemia-reperfusion synaptic plasticity cyclic adenosine monophosphate protein kinase A brain derived neurotrophic factor |
