Schizandrin B attenuates angiotensin II induced endothelial to mesenchymal transition in vascular endothelium by suppressing NF-κB activation
| Autor: | Guang Liang, Gaojun Wu, Jianchang Qian, Zhengxian Wang, Jingying Wang, Weijian Huang, Taiwei Chen, Yuanyuan Qian, Shengban You |
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| Rok vydání: | 2018 |
| Předmět: |
Male
medicine.medical_treatment Anti-Inflammatory Agents Pharmaceutical Science Inflammation Pharmacology Vascular Remodeling medicine.disease_cause Lignans 03 medical and health sciences chemistry.chemical_compound Cyclooctanes Mice 0302 clinical medicine In vivo Fibrosis Drug Discovery medicine Animals Polycyclic Compounds Cells Cultured 030304 developmental biology 0303 health sciences Chemistry Angiotensin II Mesenchymal stem cell NF-kappa B p50 Subunit NF-κB medicine.disease Mice Inbred C57BL Disease Models Animal Oxidative Stress Cytokine Phenotype Complementary and alternative medicine Gene Expression Regulation 030220 oncology & carcinogenesis Molecular Medicine Cytokines Endothelium Vascular medicine.symptom Oxidative stress Signal Transduction |
| Zdroj: | Phytomedicine : international journal of phytotherapy and phytopharmacology. 62 |
| ISSN: | 1618-095X |
| Popis: | Background Angiotensin II (Ang II)-induced chronic inflammation and oxidative stress often leads to irreversible vascular injury, in which the endothelial to mesenchymal transition (EndMT) in the endothelial layers are involved. Schisandrin B (Sch B), a natural product isolated from traditional Schisandra chinensis, has been reported to exert vascular protective properties with unclear mechanism. Hypothesis/purpose This study investigated the protective effects and mechanism of Sch B against Ang II-induced vascular injury. Methods C57BL/6 mice were subcutaneous injected of Ang II for 4 weeks to induce irreversible vascular injury. In vitro, Ang II-induced HUVECs injury was used to study the underlying mechanism. The markers of EndMT, inflammation and oxidative stress were studied both in vitro and in vivo. Results Pre-administration of Sch B effectively attenuated phenotypes of vascular EndMT and fibrosis in Ang II-treated animals, accompanied with decreased inflammatory cytokine and ROS. The in vitro data from HUVECs suggest that Sch B directly targets NF-κB activation to suppress Ang II-induced EndMT and vascular injury. The activation of EndMT in the presence of Ang II is regulated by the NF-κB, a common player in inflammation and oxidative stress. Ang II-induced inflammation and oxidative stress also contributed to vascular EndMT development and Sch B inhibited inflammation/ROS-mediated EndMT by suppressing NF-κB. Conclusion EndMT contributes to vascular injury in Ang II-treated mice, and it can be prevented via suppressing NF-κB activation by Sch B treatment. These results also imply that NF-κB might be a promising target to attenuate vascular remodeling induced by inflammation and oxidative stress through an EndMT mechanism. |
| Databáze: | OpenAIRE |
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