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In SDS-PAGE experiments, EA appears to dose-dependently inhibit the FXIIIa-mediated polymerization of fibrin(ogen) as well as the formation of fibrin(ogen) 2 -AP complex which indicates that EA affects some of the physiological functions of FXIIIa

GPR35 acts a dual role and therapeutic target in inflammation

It showed severe myocardial damage (muscle fiber destruction and pyknotic nuclei) in the DOX group, consistent with other studies investigating doxorubicin-induced cardiotoxicity by increasing cardiac biomarkers in rats 46