The dipeptidyl peptidase-IV inhibitor inhibits the expression of vascular adhesion molecules and inflammatory cytokines in HUVECs via Akt- and AMPK-dependent mechanisms

A dipeptidyl peptidase-IV inhibitor improves hepatic steatosis and insulin resistance by AMPK-dependent and JNK-dependent inhibition of LECT2 expression

“…Zeng et al [32] showed that AMPK phosphorylation increases in the aortic tissue of DPP-4 inhibitor-treated ApoE -/-mice compared to normal chow-fed mice, attenuating the progression of atherosclerosis. In our previous experiments, we found that a DPP-4 inhibitor significantly reduced LPS-induced vascular adhesion molecules and inflammatory cytokine expression in human endothelial cells and inhibited foam cell formation in monocytes by activating AMPK phosphorylation [33]. Therefore, we hypothesized that the metabolically beneficial effects of DPP-4 inhibitors might be mediated by enhanced AMPK phosphorylation, with subsequent downregulation of LECT2 expression in the liver.…”

Dipeptidyl peptidase-4 inhibitor gemigliptin protects against vascular calcification in an experimental chronic kidney disease and vascular smooth muscle cells

“…In addition, gemigliptin reduced lipopolysaccharide (LPS)-induced expression of adhesion molecules and pro-inflammatory cytokines (VCAM-1, E-selectin, TNF-α, MCP-1, IL-1ß, and IL-6) in HUVECs and inhibited LPS- and LDL-induced foam cell formation in macrophage-like THP-1 cells. These anti-inflammatory and anti-atherosclerotic effects of gemigliptin were mediated by attenuating NF-κB and JNK signaling through Akt/AMPK-dependent mechanisms [21]. However, to the best of our knowledge, this is the first study to investigate the effect of the DPP-4 inhibitor, gemigliptin on high phosphate-induced VC.…”

“…Gemigliptin improves glucose tolerance by increasing insulin secretion and decreasing glucagon secretion in vivo and in vitro [20]. Previous studies have reported on the pleiotropic effect of gemigliptin, besides its glucose lowering effect, including inhibition of LPS-induced pro-inflammatory effects in vascular endothelial cells by attenuating NF-kappaB and JNK signaling via Akt/AMPK-dependent mechanisms [21], and protection against renal interstitial fibrosis in a mouse model of ureteral obstruction [22]. However, there are few studies on the effects of gemigliptin on VC.…”

The Ca2+ mobilisation and the inhibition of akt reduced the binding of PEO-1 cells to fibronectin

“…26 Our results clearly indicated that increased calcium levels in the cytoplasm of PEO-1 cells by either extracellular or intracellular stores was essential for the binding of these cells to fibronectin. Increasing intracellular calcium in PEO-1 cells reduced cell adhesiveness and also PKB/Akt is a serine/threonine kinase that has an important role in cell survival, cell proliferation, invasion, and adhesion to the ECM in various types of cells such as human umbilical vein endothelial cells 27 , breast cancer cell 28 , and lung adenocarcinoma. 29 The overexpression of PI3K/Aktrelated genes has been observed in ovarian cancer tissues.…”