Effects of dihydroartemisinin on cardiac fibroblast activity induced by angiotensin II

Dihydroartemisinin is currently now being studied for the treatment of diseases. The mechanism of action of dihydroartemisinin on cardiovascular diseases is unclear. We explored the effect of dihydroartemisinin on the activity of cardiac fibroblasts and the underlying mechanism. The cardiac fibroblasts were divided into blank control group, dihydroartemisinin group, vascular angiotensin II (AngII) group and angiotensin II+dihydroartemisinin group followed by analysis of cell proliferation, Col I and FN levels, and the levels of TGF-β1, α-SMA and IGF-I. The morphology of myocardial fibroblasts was spindle-shaped. Further immunofluorescence staining assessed positive expression of Vimentin of the myocardial fibroblasts and no expression of α-SMA, which confirmed the successful culture of the myocardial fibroblasts. Overexpression of AngII significantly promoted the proliferation ability of mouse cardiac fibroblasts, which was significantly reduced after dihydroartemisinin treatment. As shown by RT-qPCR, TGF-β1, α-SMA and IGF-I levels in AngII mice increased, while their levels reduced after dihydroartemisinin intervention. After overexpression of AngII in cardiomyocytes, cell proliferation and colonies formation increased and decreased after dihydroartemisinin treatment, suggesting that dihydroartemisinin inhibited the growth of cardiomyocytes. It showed that dihydroartemisinin could alleviate the expression of AngII-induced activation markers of mouse cardiac fibroblasts. Therefore, our research confirms that dihydroartemisinin plays an important role in anti-myocardial fibrosis, mainly through regulating the expression of TGF-β1.