期刊
FRONTIERS IN PHARMACOLOGY
卷 8, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2017.00464
关键词
atherosclerosis; tumor necrosis factor-alpha; inflammation; ginsenoside Rb1; apoptosis
资金
- National Natural Science Foundation of China [81374011]
- CAMS Innovation Fund for Medical Sciences (CIFMS) [2016-I2M-1-012]
- Special Project of the National Traditional Chinese Medicine Industry of China [201507004]
It is currently believed that inflammation plays a central role in the pathophysiology of atherosclerosis. Oxidative stress and redox-sensitive transcription factors are implicated in the process. Ginsenoside Rb1, a major active ingredient in processed Radix notoginseng, has attracted widespread attention because of its potential to improve cardiovascular function. However, the effects of ginsenoside Rb1 on tumor necrosis factor-alpha (TNF-alpha)-induced vascular endothelial cell injury and the underlying molecular mechanisms have never been studied. This study showed that TNF-alpha-induced oxidative stress, inflammation and apoptosis in human umbilical vein endothelial cells (HUVECs) could be attenuated by ginsenoside Rb1 pretreatment. Using JC-1, Annexin V/PI and TUNEL staining, and a caspase-3 activity assay, we found that Rb1 provided significant protection against TNF-alpha-induced cell death. Furthermore, Rb1 pretreatment could inhibit TNF-alpha-induced ROS and MDA production; increase the activities of SOD, CAT, and GSH-Px; and decrease the levels of IL-1 beta, IL-6, VCAM-1, ICAM-1, VEGF, MMP-2 and MMP-9. Importantly, the cytoprotective effects of Rb1 were correlated with NF-kappa B signaling pathway inhibition. Additionally, we found that Rb1 may suppress the NF-kappa B pathway through p-38 and JNK pathway activation, findings supported by the results of our experiments involving anisomycin (AM), a JNK and p38 activator. In conclusion, this study showed that ginsenoside Rb1 protects HUVECs from TNF-alpha-induced oxidative stress and inflammation by inhibiting JNK and p38. This inhibition suppressed NF-kappa B signaling and down-regulated the expression of inflammatory factors and apoptosisrelated proteins.
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