Abstract Objective To study the role of tranilast in the pathogenesis of myocardiac fibrosis in viral myocarditis.Methods Seventy-two BALB/C mice were randomly divided into control, model and intervention groups (n=24 each). Mice in the model and intervention groups were infected with Coxsackievirus B3 to induce viral myocarditis.The intervention group was given with tranilast (200 mg/kg) by gavage until sacrifice for sampling, while the other twogroups were administered with the same volume of normal saline. Cardiac tissues were obtained from 8 mice on 7, 14and 28 days after modeling. The mast cell number was observed by toluidine blue staining and thionine staining. Thecardiac tissues were stained with hematoxylin and eosin as well as masson trichrome to observe the pathological changesin cardiac tissues. The mRNA and protein expression of osteopontin and transforming growth factor-β1 was measuredby RT-PCR and immunohistochemistry respectively. Results In the model group, the mRNA and protein expression ofosteopontin reached the highest level on the 7th day, decreasing from the 14th day, and became to the least on the 28thday; while the expression of TGF-β1 increased from the 7th day, reaching a peak on the 14th day, and decreased slightlyon the 28th day. The mRNA and protein expression of TGF-β1 and OPN was lower in the intervention group thanthe model group (P<0.05), but higher than the control group (P<0.05). The expression of OPN mRNA was positivelycorrelated to the number of mast cells. Conclusions Tranilast can reduce myocardial fibrosis by decreasing the numberof mast cells, inhibiting the expression of TGF-β1 and OPN.
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