Isolariciresinol-9'-O-α-L-arabinofuranoside protects against hydrogen peroxide‑induced apoptosis of human umbilical vein endothelial cells via a PI3K/Akt/Bad‑dependent pathway

Abstract

Isolariciresinol-9'-O-α-L-arabinofuranoside (MWS‑19) isolated from Pinus massoniana Lamb. Fresh pine needles is the major ingredient of the Songling Xuemaikang capsule therapy used for hypertension. The present study aimed to investigate the effects and underlying mechanisms of MWS‑19 on hydrogen peroxide (H2O2)‑induced apoptosis in human umbilical vein endothelial cells (HUVECs). To investigate the effect of MWS‑19 on apoptosis in HUVECs, an oxidative stress‑induced apoptosis model was established in HUVECs using H2O2, and the present study performed Hoechst 33258 staining and a Cell Counting Kit‑8 (CCK‑8) assay. Furthermore, western blot analysis was also performed to investigate the underlying mechanism of the effects of MWS‑19 on the model. The results demonstrated that MWS‑19 reversed the effects of H2O2 on cell apoptosis at a concentration range of 15.6‑250 µg/ml, with dose‑dependent increases in cell growth. Hoechst staining indicated that 500 µM H2O2 induced HUVEC apoptosis, and MWS‑19 markedly protected HUVECs against apoptosis at 31.3, 62.5 and 125 µg/ml. Furthermore, the protein expression of phosphatidylinositol 3‑kinase (PI3K), phosphorylated‑Akt and Bcl‑2‑associated agonist of cell death (Bad) were increased, and reduced caspase‑3 activation was observed, following treatment with MWS‑19 in H2O2‑treated HUVECs. Additionally, the PI3K inhibitor wortmannin attenuated PI3K/Akt/Bad signaling induced by MWS‑19 treatment and neutralized the effect of MWS‑19 on the growth of HUVECs. In conclusion, the results of the present study indicate that MWS‑19 may protect against H2O2‑induced HUVEC apoptosis via the PI3K/Akt/Bad signaling pathway. MWS‑19 may serve an important role in the prevention of oxidative damage in vascular endothelial cells in hypertension patients.

Differentiation of human induced pluripotent stem cells to authentic macrophages using a defined, serum-free, open-source medium

“…Secondly, LC-MS analysis indicated the potential presence of several undisclosed molecules in the commercial serum-free alternative medium, XVIVO 15, some of which could inhibit, or polarize the macrophage response if present. Our analysis putatively identified isolariciresinol 9′-O-alpha-L-arabinofuranoside, a lignan glycoside, which is known to have anti-inflammatory effects ( Liu et al., 2018 ), as well as methyl glucosinolate and dithionous acid. While the precise functions of these molecules are unknown, it is worth noting that indole glucosinolates have been reported to have potent anti-inflammatory effects ( Vo et al., 2014 ).…”

Reduced expression of microRNA‑199a‑3p is associated with vascular endothelial cell injury induced by type 2 diabetes mellitus

“…The PI3K/AKT signaling pathway is associated with the physiological and pathological processes of the body and has important regulatory functions for cell survival, apoptosis and the synthesis and secretion of inflammatory factors (36). It has been reported that PI3K/AKT and its downstream NF-κB signaling pathway promote proliferation, migration and tube formation in endothelial cells (37). Netrin-1 regulates high glucose-induced vascular endothelial cell damage and angiogenesis via the PI3K/AKT/eNOS signaling pathway (38), while phosphocreatine protects vascular endothelial cells from oxidative stress-induced apoptosis through the PI3K/AKT/eNOS and NF-κB signaling pathways (39).…”

2,5-Hexanedione mediates neuronal apoptosis through suppression of NGF via PI3K/Akt signaling in the rat sciatic nerve

“…The expression and phosphorylation of Akt, through PI3K activation, prevent the apoptosis that is induced by the inhibition of Akt phosphorylation [18–20]. Following Akt phosphorylation, the activation of the PI3K/Akt signaling pathway is mediated by Bcl-2 phosphorylation, followed by subsequent inhibition of Bcl-2 and Bad phosphorylation [21–23]. Phosphorylated Bad then binds to the 14-3-3 protein, releasing Bcl-xL in to the cytoplasm.…”