Protective Effects of Total Flavones of Elaeagnus rhamnoides (L.) A. Nelson against Vascular Endothelial Injury in Blood Stasis Model Rats - PubMed (original) (raw)

Protective Effects of Total Flavones of Elaeagnus rhamnoides (L.) A. Nelson against Vascular Endothelial Injury in Blood Stasis Model Rats

Zhicheng Wei et al. Evid Based Complement Alternat Med. 2017.

Abstract

The aim was to evaluate the protective effects of total flavones of Elaeagnus rhamnoides (L.) A. Nelson (TFE) against vascular endothelial injury in blood stasis model rats and explore the potential mechanisms preliminarily. The model of blood stasis rat model with vascular endothelial injury was induced by subcutaneous injection of adrenaline combined with ice-water bath. Whole blood viscosity (WBV), histological examination, and prothrombin time (PT), activated partial thromboplastin time (APTT), and fibrinogen (FIB) were measured. Meanwhile, the levels of Thromboxane B2 (TXB2), 6-keto-PGF1_α_ , von Willebrand factor (vWF), and thrombomodulin (TM) were detected. In addition, Quantitative Real-Time PCR (qPCR) was performed to identify PI3K, Erk2, Bcl-2, and caspase-3 gene expression. The results showed that TFE can relieve WBV, increase PT and APTT, and decrease FIB content obviously. Moreover, TFE might significantly downregulate the levels of TXB2, vWF, and TM in plasma and upregulate the level of 6-keto-PGF1_α_ in plasma. Expressions of PI3K and Bcl-2 were increased and the expression of caspase-3 was decreased by TFE pretreatment in the rat model. Consequently, the study suggested that TFE may have the potential against vascular endothelial injury in blood stasis model rats induced by a high dose of adrenaline with ice-water bath.

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Figures

Figure 1

Figure 1

Typical high-performance liquid chromatography profile of three known standards (a) and total flavonoid aglycones obtained by hydrolyzing (b) at an absorbance of 370 nm.

Figure 2

Figure 2

Effects of TFE on whole blood viscosity (WBV) at various shear rates. n = 6, ##P < 0.01 compared with control group. P < 0.05, ∗∗ P < 0.01 compared with model group. Highly significant change (P < 0.01) was recorded at all shear (ranging from 1 to 200 s−1), rates between control and model group (a). WBV at 1, 5, 50, 100, and 200 s−1 rates (b–f).

Figure 3

Figure 3

Effect of TFE in pathological photomicrograph of rats aorta: pathological photomicrograph of rats stained by hematoxylin and eosin (H.E. ×400).

Figure 4

Figure 4

Effect of TFE on PT (a), APTT (b), and FIB (c). n = 6, ##P < 0.01 compared with control group. P < 0.05, ∗∗ P < 0.01 compared with model group.

Figure 5

Figure 5

Determination of vWF (a) and TM (b) in the plasma. n = 6, ##P < 0.01 compared with control group; ∗∗ P < 0.01 compared with model group.

Figure 6

Figure 6

The mRNA expressions of PI3K (a), Erk2 (b), Bcl-2 (c), and caspase-3 (d). n = 6, ##P < 0.01 compared with control group. n = 6, P < 0.05, ∗∗ P < 0.01 compared with model group.

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References

    1. Chen K.-J. Blood stasis syndrome and its treatment with activating blood circulation to remove blood stasis therapy. Chinese Journal of Integrative Medicine. 2012;18(12):891–896. doi: 10.1007/s11655-012-1291-5. - DOI - PubMed
    1. Berry C. N., Girard D., Lochot S., Lecoffre C. Antithrombotic actions of argatroban in rat models of venous, ‘mixed’ and arterial thrombosis, and its effects on the tail transection bleeding time. British Journal of Pharmacology. 1994;113(4):1209–1214. doi: 10.1111/j.1476-5381.1994.tb17126.x. - DOI - PMC - PubMed
    1. Rosendaal F. R. Risk factors for venous thrombotic disease. Thromb Haemost. 1999;82(2):610–619. - PubMed
    1. McGovern V. J. Reactions to injury of vascular endothelium with special reference to the problem of thrombosis. The Journal of Pathology. 1955;69(1):283–293. doi: 10.1002/path.1700690136. - DOI - PubMed
    1. Tomaiuolo M., Brass L. F., Stalker T. J. Regulation of platelet activation and coagulation and its role in vascular injury and arterial thrombosis. Interventional Cardiology Clinics. 2017;6(1):1–12. doi: 10.1016/j.iccl.2016.08.001. - DOI - PMC - PubMed

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