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cy of these proteins. Our results also showed that JWBSYQF affects mitogen activated protein kinase (MAPK) and nuclear factor-κB (NF-κ signaling pathways, that are activated by IL-17 signaling. The present study suggested that JWBSYQF could attenuate AHR and airway inflammation in OVA-induced asthmatic mice. In addition, proteomics analysis revealed that suppression of IL-17 signaling pathways contributes to the therapeutic effects of JWBSYQF. The present study suggested that JWBSYQF could attenuate AHR and airway inflammation in OVA-
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