Effects of Levistilide A on Hemorheology and Endothelial Cell Injury in Rats with Blood Stasis

XiaoTong Liu; MiJia Zhang; YuJiao Li; WenLu He; GuangHua Lu; Qiong Wang; QiaoZhi Wang

doi:10.1155/2021/6595383

Effects of Levistilide A on Hemorheology and Endothelial Cell Injury in Rats with Blood Stasis

Evid Based Complement Alternat Med. 2021 Dec 2:2021:6595383. doi: 10.1155/2021/6595383. eCollection 2021.

Authors

XiaoTong Liu^{1

2}, MiJia Zhang², YuJiao Li², WenLu He², GuangHua Lu³, Qiong Wang^{2

4}, QiaoZhi Wang¹

Affiliations

¹ Department of Histology and Embryology, School of Basic Medical Sciences, Southwest Medical University (SWMU), Luzhou 646000, Sichuan, China.
² Sino-Portugal TCM International Cooperation Center, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
³ School of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, Sichuan, China.
⁴ Institute of Food Science and Technology, Chinese Academy of Agricultural Sciences (CAAS), Beijing 100193, China.

Abstract

Background: Vascular endothelial cell injury is not only the initiating factor of cardiovascular and cerebrovascular diseases but also the essence of blood stasis. Levistilide A (LA), a natural component isolated from the traditional Chinese herb, Ligusticum chuanxiong Hort, has traditional effects on improving blood circulation and removing stasis. In this study, the effects and potential mechanisms of LA in the rat model of blood stasis and the mechanism in endothelial cell injury have been explored.

Materials and methods: In this experiment, the effects of LA on the model of acute blood stasis in rats were explored. The blood samples were collected for the measurement of coagulation and hemorheological indices, and the carotid arteries were also excised from rats for hematoxylin-eosin (HE) staining and immunohistochemistry (IHC). In addition, the improvement effects of LA on the H₂O₂-induced human umbilical vein endothelial cell (HUVEC) injury model were evaluated. And the cell viability detection was conducted by the CCK8 assay, and the pathway-related protein expressions were detected by western blotting.

Results: In vivo, compared with the model group, the treatment of LA (10 mg/kg) could reduce the FIB (fibrinogen) content (P < 0.01), increase the INR (international normalized ratio) and PT (prothrombin time) (P < 0.01), and reduce the plasma viscosity (P < 0.05) and whole blood viscosities of low, medium, and high shear rates in the blood of blood stasis model rats (P < 0.01). In vitro, the cell viability in the LA-pretreated group was higher than that of the model group (P < 0.05). The expression levels of PI3K, AKT, and eNOs in the LA-pretreated group were increased (P < 0.01) as compared to the model group.

Conclusion: These findings demonstrated that LA has the ability to improve blood hypercoagulation and blood viscosity, and enhance the viability of cells. It is more likely that it exerts a protective effect on the endothelial cell through the PI3K-AKT-eNOs pathway. These results indicate LA will be a potential candidate to cure blood stasis with endothelial cell injury.