Journal
CNS NEUROSCIENCE & THERAPEUTICS
Volume 19, Issue 4, Pages 252-261Publisher
WILEY
DOI: 10.1111/cns.12068
Keywords
Akt; Apoptosis; Free fatty acid; Glutathione; Human brain vascular endothelial cells; Oxidative stress
Categories
Funding
- National Natural Science Foundation of China [81170322]
- Shanghai Natural Science Foundation of China [11ZR1405300]
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Aims The damage of human brain vascular endothelial cells (HBVECs) is the key pathogenesis of diabetes-associated cerebral vascular complications. The aim of this study was to elucidate the effects of glutathione (GSH) on free fatty acids (FFAs)-induced HBVECs apoptosis, oxidative stress, and the involved possible signaling pathway. Methods After culturing HBVECs for 72h with GSH and FFAs, we determined cell proliferation by CCK8, detected apoptosis by caspase-3 and Annexin V-FITC/PI staining, and judged oxygen stress by determining the reactive oxygen species (ROS) and the mitochondrial membrane potential (MMP). We investigated whether the Akt pathway was involved in FFAs-induced signaling pathway alteration and whether GSH influenced the above effects. Results After being cultured in 200M FFAs for 72h, the HBVECs proliferation significantly decreased; HBVECs apoptosis increased; the ROS levels increased; and the HBVECs MMP subsequently decreased. FFAs induced a significant decrease in phosphorylated active Akt. These alterations were obviously prevented when 1mM GSH was added to culture medium containing FFAs, and the above effects of GSH were blocked by Akt inhibitor. Conclusion GSH may prevent FFAs-induced HBVECs damage, oxidative stress, and apoptosis through activating the Akt pathway.
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