【摘 要】
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Danshen-Chuanxiongqin Injection(DCI)is a commonly used traditional Chinese medicine for the treatment of cereb-ral ischemic stroke in China.However,its underlying mechanisms remain completely understood.The current study was designed to explore the protec
【机 构】
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Pharmaceutical Informatics Institute,College of Pharmaceutical Sciences,Zhejiang University,Hangzhou
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Danshen-Chuanxiongqin Injection(DCI)is a commonly used traditional Chinese medicine for the treatment of cereb-ral ischemic stroke in China.However,its underlying mechanisms remain completely understood.The current study was designed to explore the protective mechanisms of DCI against cerebral ischemic stroke through integrating whole-transcriptome sequencing coupled with network pharmacology analysis.First,using a mouse model of cerebral ischemic stroke by transient middle cerebral artery occlusion(tMCAO),we found that DCI(4.10 mL·kg-1)significantly alleviated cerebral ischemic infarction,neurological defi-cits,and the pathological injury of hippocampal and cortical neurons in mice.Next,the whole-transcriptome sequencing was per-formed on brain tissues.The cerebral ischemia disease(CID)network was constructed by integrating transcriptome sequencing data and cerebrovascular disease-related genes.The results showed CID network was imbalanced due to tMCAO,but a recovery regulation was observed after DCI treatment.Pathway analysis of the key genes with recovery efficiency showed that the neuroinflammation sig-naling pathway was highly enriched,while the TLR2/TLR4-MyD88-NF-κB pathway was predicted to be affected.Consistently,the in vivo validation experiments confirmed that DCI exhibited protective effects against cerebral ischemic stroke by inhibiting neuroinflam-mation via the TLR2/TLR4-MyD88-NF-κB pathway.More interestingly,DCI markedly suppressed the neutrophils infiltrated into the brain parenchyma via the choroid plexus route and showed anti-neuroinflammation effects.In conclusion,our results provide depend-able evidence that inhibiting neuroinflammation via the TLR2/TLR4-MyD88-NF-κB pathway is the main mechanism of DCI against cerebral ischemic stroke in mice.
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