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Open AccessArticle

Ethyl Rosmarinate Protects High Glucose-Induced Injury in Human Endothelial Cells

1
Department of Pharmacology of Chinese Materia Medica, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China
2
Jiangsu Key Laboratory of TCM Evaluation and Translational Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China
3
Department of Natural Medicinal Chemistry, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China
4
Natural Products Laboratory, State Key Laboratory of Tea Plant Biology and Utilization, Anhui Agricultural University, Hefei 230036, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this study.
Molecules 2018, 23(12), 3372; https://doi.org/10.3390/molecules23123372
Received: 7 September 2018 / Revised: 29 November 2018 / Accepted: 18 December 2018 / Published: 19 December 2018
Ethyl rosmarinate (RAE) is one of the active constituents from Clinopodium chinense (Benth.) O. Kuntze, which is used for diabetic treatment in Chinese folk medicine. In this study, we investigated the protective effect of RAE on high glucose-induced injury in endothelial cells and explored its underlying mechanisms. Our results showed that both RAE and rosmarinic acid (RA) increased cell viability, decreased the production of reactive oxygen species (ROS), and attenuated high glucose-induced endothelial cells apoptosis in a dose-dependent manner, as evidenced by Hochest staining, Annexin V–FITC/PI double staining, and caspase-3 activity. RAE and RA both elevated Bcl-2 expression and reduced Bax expression, according to Western blot. We also found that LY294002 (phosphatidylinositol 3-kinase, or PI3K inhibitor) weakened the protective effect of RAE. In addition, PDTC (nuclear factor-κB, or NF-κB inhibitor) and SP600125 (c-Jun N-terminal kinase, or JNK inhibitor) could inhibit the apoptosis in endothelial cells caused by high glucose. Further, we demonstrated that RAE activated Akt, and the molecular docking analysis predicted that RAE showed more affinity with Akt than RA. Moreover, we found that RAE inhibited the activation of NF-κB and JNK. These results suggested that RAE protected endothelial cells from high glucose-induced apoptosis by alleviating reactive oxygen species (ROS) generation, and regulating the PI3K/Akt/Bcl-2 pathway, the NF-κB pathway, and the JNK pathway. In general, RAE showed greater potency than RA equivalent. View Full-Text
Keywords: ethyl rosmarinate; vascular endothelial cell; apoptosis; high glucose; rosmarinic acid ethyl rosmarinate; vascular endothelial cell; apoptosis; high glucose; rosmarinic acid
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MDPI and ACS Style

Shen, Y.-H.; Wang, L.-Y.; Zhang, B.-B.; Hu, Q.-M.; Wang, P.; He, B.-Q.; Bao, G.-H.; Liang, J.-Y.; Wu, F.-H. Ethyl Rosmarinate Protects High Glucose-Induced Injury in Human Endothelial Cells. Molecules 2018, 23, 3372.

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