Mechanism of Shengmai Injection Against Cerebral Ischemia Based on Proteomics
10.13422/j.cnki.syfjx.20250208
- VernacularTitle:基于蛋白质组学的生脉注射液抗脑缺血作用机制
- Author:
Jingtong LIU
1
;
Shaowei HU
1
;
Mengli CHANG
1
;
Jing XU
1
;
Qingqing CAI
1
;
Xinghong LI
2
;
Liying TANG
1
;
Huanhuan WANG
3
;
Hongwei WU
1
Author Information
1. Institute of Chinese Materia Medica，China Academy of Chinese Medical Sciences，Beijing 100700，China
2. School of Pharmacy，Zunyi Medical University，Zunyi 563099，China
3. Hospital of Integrated Chinese and Western Medicine，Tianjin 300100，China
- Publication Type:Journal Article
- Keywords:
Shengmai injection;
cerebral ischemia-reperfusion injury;
oxidative stress;
inflammatory response;
chloride intracellular channel protein 1 （CLIC1）
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(9):57-67
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo evaluate pharmacological effects of Shengmai injection（SMI）on cerebral ischemia and study its neuroprotective mechanism. MethodsMale specific pathogen-free （SPF） Sprague-Dawley （SD） rats were randomly divided into a sham group， a model group， a low-dose SMI group（3 mL·kg-1）， a middle-dose SMI group（6 mL·kg-1）， a high-dose SMI group（12 mL·kg-1）， and a Ginaton group（4 mL·kg-1）according to the random number table method， with 12 rats in each group. The rat model of cerebral ischemia-reperfusion（MCAO/R）was prepared via the suture method. The administration groups were intraperitoneally injected with corresponding concentrations of SMI or Ginaton injection after reperfusion， which was conducted for 3 consecutive days. The sham group and model group were administered the equivalent volume of physiological saline. The pharmacological effects of SMI on brain injury in MCAO/R rats were evaluated by neurological function scores， cerebral infarction area， hematoxylin-eosin （HE） staining， Nissl staining， terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） staining， and Western blot. The dominant link and key protein of SMI treating cerebral injury were explored using proteomic analysis. The related mechanisms of SMI were further validated using enzyme-linked immunosorbent assay （ELISA）， Western blot， and chloride ion fluorescence probe with oxygen-glucose deprivation/reoxygenation（OGD/R）-treated PC12 cells and MCAO/R rats. ResultsCompared with the sham group， the model group showed significantly increased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly decreased density of Nissl bodies and neurons（P<0.01）. Compared with the model group， the SMI groups exhibited significantly decreased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly increased density of Nissl bodies and neurons （P<0.05）. The proteomic analysis results showed that oxidative stress and inflammatory response were important processes of SMI intervening in MCAO/R injury， and the chloride intracellular channel protein 1 （CLIC1） was one of key proteins in its action network. The levels of representative indicators of oxidative stress and inflammatory response in the MCAO/R rats of the SMI groups were significantly reduced， compared with those in the model group（P<0.05， P<0.01）， and the expression levels of CLIC1 and downstream NOD-like receptor protein 3 （NLRP3） decreased （P<0.01）. In addition， the experimental results based on the OGD/R PC12 cells showed that SMI significantly increased the cell survival rate（P<0.01） and significantly decreased the intracellular chloride ion concentration（P<0.05）. ConclusionSMI has neuroprotective effects. Oxidative stress and inflammatory response are key processes of SMI intervening in MCAO/R injury. The potential mechanism is closely related to the regulation of CLIC1.
