Therapeutic Effects of Xiao Xumingtang Combined with Electroacupuncture on Cerebral Ischemia/Reperfusion Injury via NLRP3/GSDMD/Caspase-1 Pathway
10.13422/j.cnki.syfjx.20241106
- VernacularTitle:基于NLRP3/GSDMD/Caspase-1通路探究小续命汤联合电针对脑缺血/再灌注损伤的改善作用
- Author:
Wei MAO
1
;
Haiyang WU
2
;
Ying WANG
2
;
Haitao WANG
2
;
Haisheng JI
2
;
Junyu ZHANG
2
;
Chenglong LI
1
Author Information
1. Anhui University of Chinese Medicine，Hefei 230061，China
2. The Second Affiliated Hospital of Anhui University of Chinese Medicine，Hefei 230061，China
- Publication Type:Journal Article
- Keywords:
electroacupuncture;
ischemia-reperfusion;
NOD-like receptor hot protein domain related protein 3 （NLRP3）;
Xiao Xumingtang
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2024;30(19):39-47
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo comprehensively elucidate the potential mechanisms of Xiao Xumingtang （XXMT） combined with electroacupuncture （EA） collaboratively in alleviating cerebral ischemia/reperfusion （I/R） injury. MethodThe rat model of cerebral I/R injury was established using the modified suture-occluded method. Seven days after modeling， rats in the XXMT+EA groups were administered XXMT at low （15 g·kg-1）， medium （30 g·kg-1）， and high （60 g·kg-1） doses， alongside daily 20-min EA treatment （stimulating acupoints GV14 and GV20）. Cerebral infarction and neuronal damage were evaluated using the Zea Longa test score， TTC staining， and TUNEL staining. Real-time fluorescence quantitative PCR and Western blot were used to detect the expression of NOD-like receptor hot protein domain related protein 3 （NLRP3）， Gasdermin D （GSDMD）， cysteinyl aspartate specific proteinase-1 （Caspase-1）， interleukin-1β （IL-1β）， and interleukin-18 （IL-18） in the ischemic area of the cerebral cortex. ResultCompared with the sham group， the I/R group showed a significant increase in neurological deficit scores and infarct volume （P<0.01）， along with a higher apoptosis rate of cortical neurons and elevated mRNA and protein expression levels of NLRP3， GSDMD， Caspase-1， IL-1β， and IL-18 （P<0.05）. In contrast， the medium- and high-dose XXMT combined with EA treatment significantly reduced neurological deficit scores and infarct volume （P<0.01）， and decreased the apoptosis rate of cortical neurons as well as the mRNA and protein expression levels of NLRP3， GSDMD， Caspase-1， IL-1β， and IL-18 （P<0.05）. The improvement showed a dose-dependent relationship with XXMT. ConclusionThe combined use of XXMT and EA can exert neuroprotective effects by modulating the NLRP3/GSDMD/Caspase-1 signaling pathway， thereby reducing neurological deficits， minimizing brain infarct size， and improving cortical neuronal damage.
