A protective role of paeoniflorin in fluctuant hyperglycemia-induced vascular endothelial injuries through antioxidative and anti-inflammatory effects and reduction of PKCβ1
Download all files submitted through automated deposit
Author(s)
Wang, Jing-Shang
Huang, Ye
Zhang, Shuping
Yin, Hui-Jun
Zhang, Lei
Zhang, Yan-Hong
Song, Ye-Wen
Li, Dan-Dan
Date Issued
April 2019
Journal
Oxidative medicine and cellular longevity
Publisher
Hindawi
Citation
Wang, Jing-Shang, et al., "A protective role of paeoniflorin in fluctuant hyperglycemia-induced vascular endothelial injuries through antioxidative and anti-inflammatory effects and reduction of PKCβ1." Oxidative medicine and cellular longevity 2019: no. 5647219 doi 10.1155/2019/5647219 ©2019 Author(s)
Version
Final published version
Abstract
Hyperglycemia fluctuation is associated with diabetes mellitus (DM) complications when compared to persistent hyperglycemia. Previous studies have shown that paeoniflorin (PF), through its antiapoptosis, anti-inflammation, and antithrombotic properties, effectively protects against cardiovascular and cerebrovascular disease. However, the mechanism underlying the protection from PF against vascular injuries induced by hyperglycemia fluctuations remains poorly understood. Herein, we investigated the potential protective role of PF on human umbilical vein endothelial cells (HUVECs) subjected to intermittent glucose levels in vitro and in DM rats with fluctuating hyperglycemia in vivo. A remarkable increased apoptosis associated with elevated inflammation, increased oxidative stress, and high protein level of PKCβ1 was induced in HUVECs by intermittently changing glucose for 8 days, and PF recovered those detrimental changes. LY333531, a potent PKCβ1 inhibitor, and metformin manifested similar effects. Additionally, in DM rats with fluctuating hyperglycemia, PF protected against vascular damage as what has been observed in vitro. Taken together, PF attenuates the vascular injury induced by fluctuant hyperglycemia through oxidative stress inhibition, inflammatory reaction reduction, and PKCβ1 protein level repression, suggesting its perspective clinical usage. ©2019
MIT Department
Massachusetts Institute of Technology. Institute for Medical Engineering & Science
Terms of Use
Attribution 4.0 International
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1155/2019/5647219
