Cordycepin inhibits inflammatory responses through suppression of ERK activation in zebrafish

As a natural extract, cordycepin has been shown to play important regulatory roles in many life activities. In the study, the effects of cordycepin on inflammatory responses and the underlying mechanisms was explored using a zebrafish model. In the model of LPS-induced inflammation, cordycepin was found to significantly inhibited the expression of pro-inflammatory cytokines such as tnf-alpha, il-1 beta, il-6, and il-8. Using in vivo imaging model, cordycepin significantly inhibited fluorescent-labeled neutrophils migrating towards injury sites. Furthermore, results showed that the phosphorylation level of ERK protein dramatically decreased after cordycepin treatment. Meanwhile, the ERK inhibitor, PD0325901, significantly inhibited the expression of pro-inflammatory cytokines in LPS-induced inflammatory model and neutrophils migration in the caudal fin injury model. This study indicated the important roles of cordycepin in inhibiting LPS and injury-induced inflammation and preliminarily explained the role of ERK protein in this process.

Automated summary

Cordycepin, a natural extract, plays important regulatory roles in inflammation by inhibiting the expression of pro-inflammatory cytokines and neutrophil migration. The study showed that cordycepin can reduce the phosphorylation level of ERK protein, which is crucial in blocking inflammatory responses. The findings suggest the potential of cordycepin in treating LPS and injury-induced inflammation through modulating the ERK signaling pathway.