Protective effects of isorhamnetin on apoptosis and inflammation in TNF-α-induced HUVECs injury.

Abstract

Little is known about the role of isorhamnetin on endothelial cell apoptosis and inflammation when insulted by TNF-α injury. In our study, HUVECs were treated with TNF-α for 6 hours. HUVECs apoptosis were detected using flow cytometry. The expressions of ICAM-1, VCAM-1, E-selectin, NF-κB, AP-1 and eNOS were determined with western blotting or flow cytometry. The results showed TNF-α increased of apoptosis and the expression of ICAM-1, VCAM-1 and E-selectin in HUVECs, accompanied by significant augmentation of NF-κB and AP-1 expression. Pretreatment with isorhamnetin significantly reduced apoptosis in TNF-α-treated HUVECs. Moreover, isorhamnetin significantly attenuated TNF-α-induced upregulation of ICAM-1, VCAM-1, AP-1, E-selectin and NF-κB expression. Meanwhile, isorhamnetin also increased the expression of eNOS. So, isorhamnetin could suppress TNF-α-induced apoptosis and inflammation by blocking NF-κB and AP-1 signaling in HUVECs, which might be one of the underlying mechanisms for treatment of coronary heart disease.

• Authors: Tie-Long Chen, Guang-Li Zhu, Jian-An Wang, Guo-Dong Zhang, Hong-Fei Liu, Jin-Ru Chen, Yu Wang, Xiao-Long He
• Journal: International journal of clinical and experimental pathology (Int J Clin Exp Pathol) Vol. 8 Issue 3 Pg. 2311-20 ( 2015) ISSN: 1936-2625 [Electronic] United States
• PMID: 26045738 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Anti-Inflammatory Agents
• E-Selectin
• ICAM1 protein, human
• NF-kappa B
• SELE protein, human
• Transcription Factor AP-1
• Tumor Necrosis Factor-alpha
• Vascular Cell Adhesion Molecule-1
• 3-methylquercetin
• Intercellular Adhesion Molecule-1
• Quercetin
• NOS3 protein, human
• Nitric Oxide Synthase Type III

Topics

• Anti-Inflammatory Agents (pharmacology)
• Apoptosis (drug effects)
• Cells, Cultured
• Cytoprotection
• E-Selectin (metabolism)
• Human Umbilical Vein Endothelial Cells (drug effects, immunology, metabolism, pathology)
• Humans
• Inflammation (immunology, metabolism, pathology, prevention & control)
• Intercellular Adhesion Molecule-1 (metabolism)
• NF-kappa B (metabolism)
• Nitric Oxide Synthase Type III (metabolism)
• Quercetin (analogs & derivatives, pharmacology)
• Signal Transduction (drug effects)
• Time Factors
• Transcription Factor AP-1 (metabolism)
• Tumor Necrosis Factor-alpha (pharmacology)
• Vascular Cell Adhesion Molecule-1 (metabolism)