Astragaloside IV prevents high glucose-induced cell apoptosis and inflammatory reactions through inhibition of the JNK pathway in human umbilical vein endothelial cells

Endothelial dysfunction is a key pathophysiological step in early stage diabetes mellitus (DM) macrovascular complications and is also crucial in the inflammatory mechanisms of macrovascular complications. However, there is currently no effective intervention to improve endothelial dysfunction associated with DM macrovascular complications. Astragaloside IV (AS-IV), which can be extracted from the traditional Chinese medicine Astragalus membranaceus, has potential therapeutic effects on DM and its complications. The present study evaluated the effect of AS-IV on high glucose-induced human umbilical vein endothelial cell (HUVEC) injury and its possible mechanism. The result indicated that AS-IV has a significant protective effect on high glucose-induced HUVEC injury. AS-IV could significantly promote cell proliferation, reduce apoptosis and decrease the protein and mRNA expression levels of tumor necrosis factor-α and interleukin-1β in HUVECs. Furthermore, AS-IV could decrease the expression of phosphorylated c-Jun NH(2)-terminal kinase (JNK) phosphorylated apoptosis signal-regulating kinase 1, cytochrome c, cleaved-caspase-9, cleaved-caspase-3 and the relative ratio of B-cell lymphoma-2 associated X protein/B-cell lymphoma-2 in HUVECs. In conclusion, the present study demonstrated that AS-IV could suppress apoptosis and inflammatory reactions promoted by high glucose conditions in HUVECs by inhibiting the JNK signaling pathway. These findings suggest that AS-IV could inhibit the process of endothelial dysfunction in diabetic macrovascular complications.