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ORIGINAL ARTICLE
Year : 2020  |  Volume : 6  |  Issue : 1  |  Page : 112-120

Investigation on the mode of action of the traditional chinese medical prescription-yiqihuoxue formula, an effective extravasation treatment for cerebral vascular microemboli in ApoE-/- mice


1 Department of Neurology, The Second Affiliated Hospital of Xi'an Medical University, Xi'an; Department of Emergency, Longhua Hospital Shanghai University of Traditional Chinese Medicine, Shanghai, China
2 Department of Management Science and Engineering, School of Economics and Management, Xidian University, Xi'an, China
3 Department of Preventive Treatment, Shanghai Guanghua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai, China
4 Department of Scientific Research, The Second Affiliated Hospital of Shanxi University of Chinese Medicine, Xianyang; Department of Biochemistry, The College of Basic Medicine Sciences, Shanxi University of Chinese Medicine, Xi'an, China
5 Unit of Therapeutic Chemistry and Pharmacognosy, University of Mons, Mons, Belgium

Correspondence Address:
Prof. Xu Chao
The Second Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, 712000; The College of Basic Medicine Sciences, Shaanxi University of Chinese Medicine, Xi'an, 712046
China
Prof. Zhong-Ju Xu
Shanghai Guanghua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai, 200052
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/wjtcm.wjtcm_8_20

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Objective: The objective of this study was to investigate the mechanisms underlying anti-embolism and extravasational effects of traditional Chinese medical prescription YiqiHuoxue (YQHX) formula in ApoE-/-mice with cerebral vascular microemboli. Materials and Methods: An ApoE-/-mice model with microemboli was developed by infusing fluorescently labeled heterologous fibrin-rich microparticles into the internal carotid artery of ApoE-/-gene knockout male mice through the common carotid artery. Before microemboli injection, the animals were randomly divided into four groups of 10 animals, treated daily for 6 weeks by intragastric administration: The ApoE-/-control group (physiological saline, 0.2 mL/10 g/d), YQHX group (0.2 ml/10 g/d), clopidogrel group (3 mg/kg/d), and atorvastatin group (3 mg/kg/d); a further group was constituted of normal male C57BL/6J mice (with the same genetic background as ApoE-/-mice; normal control group; no treatment; microemboli injection). The mice in each microemboli group were divided into three subgroups, the 2-h, 24-h, and 72-h subgroups, corresponding to the time after microemboli injection. Two hours (or 24 h or 72 h) after microemboli injection, the changes in aortic intima and brain tissue were analyzed by histopathology, the amounts of fluorescent emboli being measured by fluorescence microscopy image analysis. Comparison points included the microemboli induced loss of aorta functions and pathological changes, atherosclerotic plaque, brain ultrastructure and functions, and embolus extravasation. Results: Loss of aorta functions and adverse pathological changes, atherosclerotic plaque, serious damage in brain ultrastructure and functions, and reduced thrombus elimination were obviously serious in microemboli injected ApoE-/-mice. These symptoms were significantly relieved by the YQHX pretreatment: (i) the ratio of thrombus accumulation was increased with a significant decrease in thrombus extravasation in ApoE-/-mice, while YQHX induced an increased thrombus extravasation; (ii) the degree of aortic intimal thickening and brain tissue structural disorders were significantly increased in ApoE-/-mice, but overtly inhibited in the YQHX group; (iii) YQHX restored cell viability and homeostasis in the brain; (iv) YQHX regulated the expression of pro- and anti-inflammatory cytokines in the aorta; and (v) YQHX reduced cortical nerve nuclei pyknosis, edema, liquefaction, and necrosis induced by brain hypoxia, especially in the 24 h and 72 h groups. Conclusions: These findings indicate that the protective effects of YQHX on the brain against microemboli-induced injury may be attributed to the activation of extravasation mechanisms, which are involved in the cerebrovascular injury pathway and constitutively important in the progression of ischemic stroke.


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