الفهرس 
Role of angiotensin II (Ag II), transforming growth factor-?1 (TGF-?1) and ?-catenin in the potential cardioprotective effect of quercetin in experimentally induced myocardial infarction
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Abstract
Quercetin and telmisartan have proven their cardioprotective effect in several models of heart injury; however, not all mechanisms of action have been explored. The aim of the current study was to test the potential involvement of several signaling pathways of either agent or their combination on myocardial ischemia/reperfusion (I/R) model. Wistar male rats were randomly divided into normal control, quercetin (QN), telmisartan (Tel7, Tel12), and a QN+Tel12 group. Both QN and Tel12 protected heart against I/R as indicated by preventing ATP depletion and hindering I/R-induced ST elevation, Tropinin-I, CPK, and LDH. This effect could be attributed to their antioxidant capacity and anti-inflammatory effects evidenced by modulating redox imbalance (ROS, MDA, TAC, SOD) and inflammatory mediators (NF-mβ, TNFÜ, ICAM, MPO). Additionally, they decreased caspase 3 and increased Bcl-2 pointing to their anti-apoptotic effect. Moreover, to hinder the fibrotic event, Tel and QN attenuated the fibrotic marker TGFÝ. Besides blocking Ag II receptor, Tel, as well as QN, opposed the elevation of Ag II; this effect indicates the involvement of Ag II signaling pathway in the anti-inflammatory, anti-apoptotic and anti-fibrotic effects of these agents. Wnt/Ý catenin is another signaling cascade that play a role in the cardioprotective effect of both agents by preserving Ý-catenin through inhibition of GSK 3Ý. Combination regimen offered the best results by keeping these parameters within their normal levels. In conclusion, Tel and QN mediated their cardioprotective effect by the modulation of oxidative stress, inflammation, apoptosis and fibrosis via Wnt/Ý catenin, GSK3Ý, Ag II and TGFÝ signaling pathways