Ethyl pyruvate attenuates delayed experimental cerebral vasospasm following subarachnoid haemorrhage in rats: possible role of JNK pathway

The pathophysiology of delayed cerebral vasospasm (CVS) after subarachnoid haemorrhage (SAH) is multifaceted and involves endothelial apoptosis and inflammation. Ethyl pyruvate (EP) could attenuate early brain injury following SAH via anti-inflammation and inhibition of the c-Jun N-terminal kinase (JNK) signalling pathway. However, the role of EP in the delayed CVS has yet to be determined. In this study, we examined the effect of EP on endothelial apoptosis and inflammation and explore possible signalling pathways. We found that EP could significantly attenuate the delayed CVS. Possible mechanisms include a decrease in the endothelial cell apoptosis of the basilar artery and alleviation of endothelial inflammation. The JNK signalling pathway may play an important role in the neuroprotective effects of EP on delayed CVS. The results suggest that EP may be a possible therapy for delayed CVS, and the JNK signalling pathway should be targeted for therapeutic purposes in the future.

• Publication year

  2018

• Venue

  RSC Advances

• Publication date

  2018-02-14

• Fields of study

  Medicine

• Identifiers
  DOI 10.1039/c7ra10801jPMID 35539121PMCID 9078488
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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