Triptolide Promote Neuronal Plasticity with Cerebral Ischemia-reperfusion Injury by Regulating the cAMP/PKA/BDNF Signaling Pathway
10.13748/j.cnki.issn1007-7693.20221977
- VernacularTitle: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
- Author:
Bingtao MU
1
;
Minfang GUO
1
;
Jingwen YU
1
;
Huiyu ZHANG
2
Author Information
1. Shanxi Datong University Medical College
2. Shanxi Datong University College of Traditional Chinese Medicine Health Service, Datong 037009, China
- Publication Type:Journal Article
- Keywords:
triptolide ； ischemia-reperfusion ；synaptic plasticity ； cyclic adenosine monophosphate ； protein kinase A ； brain derived neurotrophic factor
- From:
Chinese Journal of Modern Applied Pharmacy
2024;41(7):911-916
- CountryChina
- Language:Chinese
-
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.
