Abstract
Background: In our previous study, we found that the combination of a traditional Chinese medicine (TCM) and swimming could prevent atherosclerosis through a synergistic interaction. However, whether the combined application of active components from the fruit of Crataegus pinnatifida Bge. Var. major N.E. Br. and the root of Salvia miltiorrhiza Bge. (CPSM) and swimming has been effective in the prevention and treatment of focal cerebral infraction remained unclear. This work aimed to conduct detailed investigation on the joint effects of CPSM extract with swimming on focal cerebral infraction in rats and its underlying mechanisms.Method: A photochemical method of the combination of Rose Bengal (RB) injection and cold-light source irradiation was performed to establish the rat focal cerebral thrombosis model. The pathological changes of the brain were observed by a DCP-7030 laser multifunction machine, and the protein levels of von Willebrand factor (vWF), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) were detected by Western blotting. Blood samples were collected to assay tissue plasminogen activator (t-PA), plasminogen activator inhibitor type-1 (PAI-1), endothelin-1 (ET-1), 6-keto-prostaglandin F1α (6-keto-PGF1α), and thromboxane B2 (TXB2). Finally, the gene expression of t-PA, PAI-1, and ICAM-1 in human umbilical vein endothelial cells (HUVECs) stimulated by tumor necrosis factor-α (TNF-α) was assayed via real-time (RT) quantitative PCR (qPCR).Results: The joint effects of CPSM extract and swimming demonstrated significant interactions, which including increased blood perfusion, increased serum t-PA and 6-keto-PGF1α, decreased serum PAI-1 and TXB2, decreased protein levels of vWF, VCAM-1 and ICAM-1, and decreased ICAM-1 gene expression.Conclusion: This research demonstrated that the combined therapy of CP and SM extracts with swimming could prevent focal cerebral infraction through interactions on the regulation of vascular endothelial functions and inflammatory factors. It stresses the promising effects of the drugs and shear stress of blood flow in prevention and treatment of thrombosis. The mechanism may be related to regulating the protein expression of vWF, VCAM-1, and ICAM-1, and downregulating the gene expression of ICAM-1.
Highlights
Cerebral infraction commonly occurs because of arterial thrombosis, which results in occlusion in the blood vessel and generates hypoxia in the brain (Strong et al, 2007)
Primary polyclonal antibodies against ICAM-1 and VCAM-1 were from Absin Bioscience Inc. (Shanghai, China). vWF polyclonal primary antibody was purchased from Proteintech Group, Inc. (Chicago, United States). β-actin polyclonal primary antibody was from Beijing biosynthesis biotechnology Co., Ltd. (China)
Our results indicated that the joint effect of swimming combined with CPSM extract increased t-PA release (F = 2.788, p = 0.035) and decreased the level of PAI-1 (F = 4.744, p = 0.002)
Summary
Cerebral infraction commonly occurs because of arterial thrombosis, which results in occlusion in the blood vessel and generates hypoxia in the brain (Strong et al, 2007). Blood flow analysis in the cerebrovascular has become an important research topic in biomechanics. These blood vessels have complex geometry, including non-linear carves, constantly changing cross-sections, and several branches (Yan et al, 2020). A growing body of evidence has revealed that the impact of blood flow on endothelial cells (ECs) is primarily determined by two flow conditions: steady laminar flow and disturbed flow The former is a protective factor, whereas the latter is an undesirable factor through thrombosis, inflammatory response, and endothelial dysfunction (Tanioka et al, 2019), indicating that disturbed flow plays an important role in the procession of cerebral infraction. (CPSM) and swimming has been effective in the prevention and treatment of focal cerebral infraction remained unclear. This work aimed to conduct detailed investigation on the joint effects of CPSM extract with swimming on focal cerebral infraction in rats and its underlying mechanisms
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