Changes in nitric oxide,angiotensinⅡ,angiopoietin-like protein 4 mRNA,neuregulin 1 mRNA,and platelet endothelial cell adhesion molecule-1 in rats with acute blood stasis induced by high-molecular-weight dextran  

作　　者：Feng Yu Zhang Junxiu Li Shaodan Liu Yi Zhang Yin Guo Yunxia Yang Minghui 

机构地区：[1]Institute of Traditional Chinese Medicine,Chinese People's Liberation Army General Hospital,Beijing 100853,China

出　　处：《Journal of Traditional Chinese Medicine》2017年第6期846-853,共8页中医杂志（英文版）

基　　金：Supported by the National Program on Key Basic Research Project(973 Program:Study of Choroid Theory Based On Cardiac Cerebrovascular Disease.No.2012CB518601)

摘　　要：OBJECTIVE: To investigate the influence of acute blood stasis on nitric oxide(NO), angiotensin Ⅱ(Ang Ⅱ), angiopoietin-like protein 4(ANGPTL4)m RNA, neuregulin 1(NRG-1) m RNA, and platelet endothelial cell adhesion molecule-1(PECAM-1) in rats with stasis induced by high-molecular-weight dextran(HMWD).METHODS: Seventy-five Sprague Dawley rats were divided randomly into five groups(n = 15 in each group): control group, immediate group, 1 h group,3 h group, and 6 h group. A model of acute blood stasis was established via injection of HMWD into the tail vein. After performing electrocardiogram at the predetermined times according to the grouping, we collected blood and cardiac samples for hematoxylin-eosin(HE) staining and histopathological examination via transmission electron microscopy. Enzyme-linked immunosorbent assay was used to detect plasma levels of NO, AngⅡ, and fibrinogen. Real-time polymerase chain reaction was used to detect the expression of ANGPTL4 m RNA and NRG-1 m RNA. Immunohistochemical methods were used to detect PECAM-1 protein expression.RESULTS: The rat model of blood stasis showed blood retention in the capillary lumens. The ST segment showed gradual elevation, and was still elevated at 3 and 6 h after induction of blood stasis.HE staining showed myocardial cell necrosis and dissolution after modeling, along with basement membrane rupture and mitochondrial structural damage. Transmission electron microscopy showed endothelial cell swelling and an increase in absorption vesicles immediately after modeling. Endothelial cell apoptosis was increased at 3 and 6 h after modeling. Cardiac muscle fibers were disordered and intercalated discs were blurred immediately after modeling. There were massive numbers of dissolved cardiac muscle fibers, ruptured basement membranes, and mitochondrial structural damage at 3 and 6 h after modeling. NO plasma concentration was significantly reduced immediately and 1 h after modeling, while it was increased at 3 and 6 h.AngⅡ plasma concentration was decreasedOBJECTIVE: To investigate the influence of acute blood stasis on nitric oxide(NO), angiotensin Ⅱ(Ang Ⅱ), angiopoietin-like protein 4(ANGPTL4)m RNA, neuregulin 1(NRG-1) m RNA, and platelet endothelial cell adhesion molecule-1(PECAM-1) in rats with stasis induced by high-molecular-weight dextran(HMWD).METHODS: Seventy-five Sprague Dawley rats were divided randomly into five groups(n = 15 in each group): control group, immediate group, 1 h group,3 h group, and 6 h group. A model of acute blood stasis was established via injection of HMWD into the tail vein. After performing electrocardiogram at the predetermined times according to the grouping, we collected blood and cardiac samples for hematoxylin-eosin(HE) staining and histopathological examination via transmission electron microscopy. Enzyme-linked immunosorbent assay was used to detect plasma levels of NO, AngⅡ, and fibrinogen. Real-time polymerase chain reaction was used to detect the expression of ANGPTL4 m RNA and NRG-1 m RNA. Immunohistochemical methods were used to detect PECAM-1 protein expression.RESULTS: The rat model of blood stasis showed blood retention in the capillary lumens. The ST segment showed gradual elevation, and was still elevated at 3 and 6 h after induction of blood stasis.HE staining showed myocardial cell necrosis and dissolution after modeling, along with basement membrane rupture and mitochondrial structural damage. Transmission electron microscopy showed endothelial cell swelling and an increase in absorption vesicles immediately after modeling. Endothelial cell apoptosis was increased at 3 and 6 h after modeling. Cardiac muscle fibers were disordered and intercalated discs were blurred immediately after modeling. There were massive numbers of dissolved cardiac muscle fibers, ruptured basement membranes, and mitochondrial structural damage at 3 and 6 h after modeling. NO plasma concentration was significantly reduced immediately and 1 h after modeling, while it was increased at 3 and 6 h.AngⅡ plasma concentration was decreased

关 键 词：Blood stasis Basic theory of TraditionalChinese Medicine Endothelial cells ANGIOTENSIN Ⅱ  NEUREGULIN-1 Antigens  CD31 

分 类 号：R228[医药卫生—中医基础理论]