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Schizandrin B Attenuates Angiotensin II Induced Endothelial to Mesenchymal Transition in Vascular Endothelium by Suppressing NF-κB Activation

Schizandrin B Attenuates Angiotensin II Induced Endothelial to Mesenchymal Transition in Vascular Endothelium by Suppressing NF-κB Activation

Shengban You, Jianchang Qian, Gaojun Wu, Yuanyuan Qian, Zhengxian Wang, Taiwei Chen, Jingying Wang, Weijian Huang, Guang Liang

Phytomedicine. 2019 Sep;62:152955.

PMID: 31146168

Abstract:

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP61281376	Schizandrin B		61281-37-6	Price

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