Neferine prevented hyperglycemia-induced endothelial cell apoptosis. - GreenMedInfo Summary
Neferine prevented hyperglycemia-induced endothelial cell apoptosis through suppressing ROS/Akt/NF-κB signal.
Endocrine. 2014 Dec ;47(3):764-71. Epub 2014 Mar 4. PMID: 24590293
Diabetes mellitus has been identified as a major risk factor for cardiovascular diseases. High glucose-induced endothelial dysfunction and apoptosis is an important pathological feature of diabetic vasculopathy. Neferine, an alkaloid ingredient in lotus seed embryo has many biological actions such as anticancer and antioxidant. But little is known about whether Neferine protects endothelial cells against high glucose-induced oxidative stress and apoptosis. The present study was conducted to investigate the preventive effects of Neferine on hyperglycemia-induced injury of human umbilical vein endothelial cells (HUVECs). Our study showed that Neferine pretreatment effectively suppressed high glucose-induced HUVECs apoptosis. Also, Neferine pretreatment inhibited the augment of reactive oxygen species (ROS) in high glucose-treated HUVECs. The changes of SOD and MDA level in high glucose-treated HUVECs were also prevented by Neferine. Further study showed that Neferine did not affect the phosphorylation of JNK and p38 in high glucose-treated HUVECs. Interestingly, Neferine markedly inhibited high glucose-induced activation of PI3K/Akt pathway in HUVECs. High glucose-induced activation of NF-κB signal was also obviously suppressed by Neferine pretreatment. Collectively, we found that Neferine inhibited high glucose-induced endothelial apoptosis via blocking ROS/Akt/NF-κB pathway, which provides the evidence for using Neferine to treat diabetic vasculopathy.