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Erschienen in:
05.10.2017 | Original articles
Ginsenoside-Rb3 inhibits endothelial–mesenchymal transition of cardiac microvascular endothelial cells
Erschienen in: Herz | Ausgabe 1/2019
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Background
We investigated the effect of Ginsenoside-Rb3 (Rb3) on the endothelial-to-mesenchymal transition (EMT) of cardiac microvascular endothelial cells (CMVECs) following coxsackievirus B3 (CVB3) infection.
Methods
CMVECs were infected with 100 TCID50 CVB3 (CVB3 group) or treated with Rb3 (Rb3 group); stably cultured CMVECs were used as control. Cells treated with the Pyk2 inhibitor TAE226 and PI3K inhibitor LY294002 were used for additional experiments. Cell viability was assessed with the Cell Counting Kit-8 (CCK8). Expression of CD31 and α‑smooth muscle actin (α-SMA) was evaluated by immunofluorescence (IF) and Western blotting (WB). Expression of Pyk2, PI3K, and AKT was assessed by real-time polymerase chain reaction (RT-PCR) and WB.
Results
Cell morphology, including cell pyknosis, and viability were significantly impaired by CVB3 infection (p < 0.05). However, the morphology of the Rb3 group was unaffected. The CCK8 assay showed that viability in the Rb3 group was increased compared with the CVB3 group (p < 0.05). Expression of CD31 decreased and α‑SMA increased in the CVB3 group compared with the control group (p < 0.05), but CD31 increased while α‑SMA decreased in the Rb3 group compared with the CVB3 group (p < 0.05). IF staining showed the same trends. The levels of Pyk2, PI3K, AKT, and CD31 were up-regulated in the Rb3 group compared with the CVB3 group, whereas α‑SMA decreased (p < 0.05). In the Pyk2-inhibitor group, PI3K, AKT, and CD31 expression was down-regulated while α‑SMA expression increased in comparison with the Rb3 group (p < 0.05). In the PI3K-inhibitor group, the levels of AKT and CD31 decreased while α‑SMA increased (p < 0.05), although the level of Pyk2 expression showed no obvious change in comparison with the Rb3 group.
Conclusion
Rb3 inhibited EMT in CMVECs following CVB3 infection via the Pyk2–PI3K–AKT signaling pathway.