Andrographolide attenuates viral myocarditis through interactions with the IL-10/STAT3 and P13K/AKT/NF-κβ signaling pathways.

Abstract

As a cardiac disease caused by the inflammation of the heart muscle, viral myocarditis (VMC) causes dilated cardiomyopathy, congestive heart failure and even death. With anti-inflammatory activities, andrographolide has been used in the treatment of various human diseases. In the present study, therapeutic effects of andrographolide on VMC were investigated using a VMC mouse model. Measurement of physiological indexes and echocardiographic examination was performed to explore the effects of andrographolide on cardiac function in mice with VMC. Levels of TNF-α, hs-CRP and cTnl in serum were measured by enzyme-linked immunosorbent assay (ELISA). Effects of andrographolide on the expression of L-10, STAT3, NF-κβ p65 and NF-κβ p50 were investigated by western blot analysis. Results indicated that andrographolide treatment reduced serum levels of TNF-α, hs-CRP and cTnl, increased the expression levels of IL-10 and STAT3 and reduced the expression levels of NF-κβ p65 and NF-κβ p50 and the phosphorylation levels of phosphoinositide 3-kinase (P13K) and AKT in the heart tissues of mice with VMC. In addition, andrographolide also increased the expression level of Iκβα in heart tissue. Therefore, it was concluded that andrographolide may inhibit the progression of VMC by interacting with the IL-10/STAT3 and NF-κβ signaling pathways.