Research Paper Volume 13, Issue 19 pp 22843—22855

Allicin protects against myocardial I/R by accelerating angiogenesis via the miR-19a-3p/PI3K/AKT axis

Allicin-mediated increase in VEGF and MMP was dependent on pPI3K. LPS stimulated Tie2 expressing macrophages were cultured in an ischemic buffer. Tie2 expressing macrophages were incubated with fluorescent dye fura-2/AM. (A) The accumulation of VEGF was noticeably visualized with fura-2/AM fluorescence in the Allicin treated Tie2 expressing macrophages. (B) the results of qPCR and Western blotting showed that Allicin treatment significantly increased the expression of the p-PI3K, p-AKT, p-mTOR, VEGF, COX2, and MMP2 in LPS stimulated Tie2 expressing macrophages compared with saline control (P P

Figure 5. Allicin-mediated increase in VEGF and MMP was dependent on pPI3K. LPS stimulated Tie2 expressing macrophages were cultured in an ischemic buffer. Tie2 expressing macrophages were incubated with fluorescent dye fura-2/AM. (A) The accumulation of VEGF was noticeably visualized with fura-2/AM fluorescence in the Allicin treated Tie2 expressing macrophages. (B) the results of qPCR and Western blotting showed that Allicin treatment significantly increased the expression of the p-PI3K, p-AKT, p-mTOR, VEGF, COX2, and MMP2 in LPS stimulated Tie2 expressing macrophages compared with saline control (P < 0.05). Furthermore, we found the opposite results that the increased p-PI3K, p-AKT, p-mTOR, VEGF, COX2, and MMP2 were reversed by inhibitor treatment (P < 0.05).