The Protective Effect of Icariin on Myocardial Injury in Viral Myocarditis Based on the Cyclic Adenosine Monophosphate-Protein Kinase a Signaling Pathway

Abstract

Viral myocarditis (VM) is an inflammatory lesion of the myocardium caused by a viral infection. Icariin has anti-viral effects, but its therapeutic effect and mechanism of VM action are still not clear. This study evaluated icariin’s intervention effect on the myocardial cAMP-PKA signaling pathway and explored the possible mechanism of icariin’s effect. The results showed that a high dose of icariin could improve VM rats’ quality of life. Icariin-treated rats had lower mortality, insignificant weight loss, and decreased CK-MB and LDH. Hematoxylin-Eosin (HE) staining to observe the pathological changes of rats. The myocardium of VM rats is severely damaged, and myocardial cells have dissolution, necrosis, degeneration, and inflammatory cell infiltration. The degree of myocardial pathology in rats after icariin treatment is less than that in VM model rats. ELISA detected the serum IL-6 and IL-10 levels, and it was found that the levels of IL-6 and IL-10 in rats after icariin treatment were lower than those in model rats. Prove that icariin plays a protective effect on cardiomyocytes. The positive expression of Fas in the myocardium was measured using the immunohistochemical method. The results demonstrated that the positive expression of Fas in rats was reduced after icariin treatment. The results proved that icariin reduced cardiomyocyte apoptosis. Western Blot detected myocardial cAMP and PKA protein content. In contrast with model rats, icariin reduced the cAMP and PKA levels of VM rats, showing that icariin reduces myocardial cell damage.