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

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
XiaoTong Liu ◽  
MiJia Zhang ◽  
YuJiao Li ◽  
WenLu He ◽  
GuangHua Lu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Viability ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Chinese Herb ◽  
Blood Stasis ◽  
Potential Candidate ◽  
Model Group ◽  
Endothelial Cell Injury ◽  
Pretreated Group

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.

scholarly journals Role of leukocyte derived elastase in vascular endothelial cell injury.

Ensho ◽  
1993 ◽  
Vol 13 (2) ◽  
pp. 139-144
Author(s):  
Hiroshi Fujita
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury

scholarly journals Microparticulate Caspase 1 Regulates Gasdermin D and Pulmonary Vascular Endothelial Cell Injury

2018 ◽  
Vol 59 (1) ◽  
pp. 56-64 ◽  
Author(s):  
Srabani Mitra ◽  
Matthew Exline ◽  
Fabien Habyarimana ◽  
Mikhail A. Gavrilin ◽  
Paul J. Baker ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury ◽  
Caspase 1

scholarly journals Blocking the REDD1/TXNIP axis ameliorates LPS-induced vascular endothelial cell injury through repressing oxidative stress and apoptosis

2019 ◽  
Vol 316 (1) ◽  
pp. C104-C110 ◽  
Author(s):  
Xuhui Hou ◽  
Songbai Yang ◽  
Jian Yin
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Reactive Oxygen Species Generation ◽  
Vascular Endothelial ◽  
Interacting Protein ◽  
Endothelial Cell Injury ◽  
Lactate Dehydrogenase Release

The aim of the present study was to investigate the potential role of regulated in development and DNA damage response 1 (REDD1) in LPS-induced vascular endothelial injury by using human umbilical vein endothelial cells (HUVECs). We observed that REDD1 expression was apparently elevated in HUVECs after exposure to LPS. Additionally, elimination of REDD1 strikingly attenuated the secretion of the proinflammatory cytokines TNF-α, IL-6, IL-1β, and monocyte chemotactic protein-1 and the endothelial cell adhesion markers ICAM-1 and VCAM-1 that was induced by LPS stimulation. Subsequently, knockdown of REDD1 augmented cell viability but ameliorated lactate dehydrogenase release in HUVECs stimulated with LPS. Meanwhile, depletion of REDD1 effectively restricted LPS-induced HUVEC apoptosis, as exemplified by reduced DNA fragmentation, and it also elevated antiapoptotic Bcl-2 protein, concomitant with reduced levels of proapoptotic proteins Bax and cleaved caspase-3. Furthermore, repression of REDD1 remarkably alleviated LPS-triggered intracellular reactive oxygen species generation accompanied by decreased malondialdehyde content and increased the activity of the endogenous antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase. Most important, depletion of REDD1 protected HUVECs against inflammation-mediated apoptosis and oxidative damage partly through thioredoxin-interacting protein (TXNIP). Collectively, these findings indicate that blocking the REDD1/TXNIP axis repressed the inflammation-mediated vascular injury process, which may be closely related to oxidative stress and apoptosis in HUVECs, implying that the REDD1/TXNIP axis may be a new target for preventing the endothelial cell injury process.

scholarly journals Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Lei Yi ◽  
Zengding Zhou ◽  
Yijuan Zheng ◽  
Mengling Chang ◽  
Xiaoqin Huang ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Inflammatory Mediator ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Promising Candidate ◽  
Neuroprotective Effects ◽  
Endothelial Cell Injury ◽  
Tnf Α

Background. Under septic conditions, LPS induced lung vascular endothelial cell (EC) injury, and the release of inflammatory mediator launches and aggravates acute lung injury (ALI). There are no effective therapeutic options for ALI. Genistein-3′-sodium sulfonate (GSS) is a derivative of native soy isoflavone, which exhibits neuroprotective effects via its antiapoptosis property. However, whether GSS protect against sepsis-induced EC injury and release of inflammatory mediators has not been determined. In this study, we found that GSS not only downregulated the levels of TNF-α and IL-6 in the lung and serum of mice in vivo but also inhibited the expression and secretion of TNF-α and IL-6 in ECs. Importantly, we also found that GSS blocked LPS-induced TNF-α and IL-6 expression in ECs via the Myd88/NF-κB signaling pathway. Taken together, our results demonstrated that GSS might be a promising candidate for sepsis-induced ALI via its regulating effects on inflammatory response in lung ECs.

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