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Objective Metabolites produced by metabolic imbalance such as free fatty acids and lipopolysaccharides can result in a state of chronic low-grade inflammation, or metabolic inflammation, which plays an important role in the pathogenesis of atherosclerosis, type 2 diabetes, non-alcoholic fatty liver disease, and obesity. The above metabolic disorders are closely related with the metabolic inflammation, which always coexist. Therefore, we proposed the concept ofmetabolic inflammatory syndrome ( MIS). According to our study, patients with two or more metabolic disorders above could be diagnosed as MIS. The current research is aimed to investigate the prevalence of MIS and its components, and to compare the clinical values of MIS and metabolic syndrome ( MS) . Methods 2 001 in patients with type 2 diabetes from 6 hospitals in Shanghai were recruited in the current multi-center cross-sectional study. The diagnostic rates of MIS and MS and their components of both syndromes were compared. Results In the patients with type 2 diabetes, the detective rate of MIS was 96. 2%, which was higher than that of MS (71. 3%). Among 4 components of MIS, atherosclerosis showed the highest detective rate (75.6%). MIS[OR=2.252(95%CI1.026-4.942),P=0.043],atherosclerosis[OR=2.726(95% CI1.953-3. 804),P<0. 001], and MS[OR=1. 915 (95%CI 1. 444-2. 540),P<0. 01] were the risk factors of coronary heart disease. Conclusion With atherosclerosis, type 2 diabetes mellitus, non-alcoholic fatty liver disease, and obesity as its 4 components, MIS has a high detective rate in patients with metabolic disorders, and seems to be more sensitive than MS to distinguish inflammation-related metabolic diseases. The concept of MIS will promote the screening and prevention of atherosclerosis in its early stage.
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AIM:To observe the improvement in the endothelial function of patients with long-term use of Shexiang Baoxin Pill(Moschus,Ginseng extract,Calculus bovis,Cortex cinnamomi,Styrax,Venenum bufonis,and Borneolum Syntheticum)(SXBXP).METHODS:Eighty patients with CHD were randomly assigned into the SXBXP group and the control group.Two groups were controlled with the usual treatment.SXBXP 2 pills,po.tid.were taken in the SXBXP group and continued for at least 6 months.The ultrasound assessment of endothelial-dependent flow-mediated vasodilation(FMD)of the brachial artery was applied in the 3rd,6th and 18th and simultaneous determination of nirtogen oxides(NO),nitricoxide synthase(NOS),superoxide dismutase(SOD),endothelin(ET)was made.RESULTS:Follow-up checkups revealed that the level of FMD and SOD in the 3rd month,the level of NO,NOS and ET in the 6th month in SXBXP group were better than those in the control group at the significant level(P＜0.05).Patient keeping on taking SXBXP up to the 18th month,the obvious improvement in the level of FMD,NO,NOS and SOD was showed(P＜0.05).CONCLUSION:Administration of SXBXP could improve endothelial function in the CHD patients significantly.
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Background and purpose:In in vivo and vitro studies, Rhodiola shows anti-cancer effect, but there were few reports about the effects of Rhodiola on growth of breast cancer and its possible mechanism. Methods:Xenograft of Human breast cancer cells MDA-MB-435 in female BALB/c nude mice were treated with and without Rhodiola extracts. The tumor volume and proliferation index (PCNA and Ki67) of the xenograft were studied.Results:After Rhodiola was given to nude mice for 4 weeks, the mean tumor volume was smaller (99.95mm 3 vs. 174.60mm 3 ) compared to untreated group,but there was no statistical significance(P=0.535). The proportion and intensity of cellular Ki-67 staining in Xenografts were decreased as compared to the untreated group, (average H-score 152.8 vs. 86, P=0.014), the same trend could be found for cellular PCNA staining, but there was no statistical significance(242 vs.210,P=0.221).Conclusions:The mechanism of anti-cancer effect of Rhodiola may be partly through inhibiting the proliferation of cancer cells in vivo.
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OBJECTIVE: To study the effect of Zhenju Jiangya Tablet (ZJ) on the injured endothelial cells and endothelium-dependent relaxation function of hyperlipidemia rabbits. METHODS: Male New Zealand rabbits were randomized into four groups: control group, hyperlipidemia group, ZJ group and sivastatin group. The endothelium-dependent relaxation function was evaluated by APV using intravascular Doppler, and the morphology of endothelial cells was detected by light microscopy and electron microscopy, and nitric oxide synthase was evaluated. RESULTS: ZJ reduced the lesions of hyperlipidemia vessels, and the APV after Ach injection of each group was (1.14+/-0.26), (1.74+/-0.59), (1.22+/-0.37) and (1.17+/-0.41) respectively. The eNOS of each group was (4.21+/-0.37), (1.43+/-0.88), (3.95+/-0.67) and (4.08+/-0.46) nmol x min(-1) x g(-1) respectively. CONCLUSION: ZJ can improve the abnormality of endothelial cells and endothelium-dependent relaxation function of hyperlipidemia.
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OBJECTIVE: To study the effect of salvianolate on the migration of endothelial cells induced by monocytes. METHODS: Transwell-boydom system was used to test the migration of endothelial cells induced by monocytes. Enzyme-linked immunosorbent assay (ELISA) and RT-polymerase chain reaction (RT-PCR) method were used to determine the effect of salvianolate on the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) and their mRNA of monocytes. RESULTS: The migration of endothelial cells induced by monocytes was facilitated by salvianolate, compared with the control. After the monocytes were treated by salvianolate for 24 hours, the expression of mRNA of VEGF and bFGF was significantly up-regulated, and the expression of VEGF and bFGF was increased. CONCLUSION: The facilitation of salvianolate on the migration of endothelial cells induced by monocytes was observed. Salvianolate stimulates the expression of VEGF and bFGF and their mRNA of monocytes, and salvianolate may have the role of inducing migration of endothelial cells by working on these two factors.
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AIM: To study the expression of endostatin in ischemic myocardium of myocardial infarction(MI) rats in various periods and the correlation with VEGF expression and microvascular density(MVD).METHODS: Thirty-two male Sprague-Dawley rats after myocardial infarction were randomly divided into 7,14,21 and 28 days group.The sham group was normal control group(eight rats in each group).The expression of endostatin,VEGF and MVD in ischemic myocardium were observed by immunohistochemistry.RESULTS: The expression of endostatin significantly increased in the ischemic myocardium after MI,peaked at 7 days,then gradually decreased at 14,21 and 28 days.The endostatin level at 28 days was the same as the shams.The changing trends of expression of endostatin in ischemic myocardium after MI were similar to that of VEGF and were significantly correlated with the MVD.CONCLUSION: The expression of endostatin increased in ischemic myocardium of myocardial infarction rats.The changing trends of endostatin were similar to that of VEGF and positively correlated with the MVD.These data suggest that endostatin may modulate ischemic myocardium angiogenesis after myocardial infarction.
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AIM:To study the role of Rhodiolae rosae in post myocardial infarction angiogenesis and its effect on extracellular regulated kinases(ERK 1/2). METHODS: The experimental myocardial infarction was made by ligation of rat left anterior descending coronary artery,and then divided into Rhodiolae group and saline group.The sham operation group and normal group were also made as control one.On the first,the 4th,the 7th and the(14th) day after the operation,rats were sacrificed and infarcted border tissue or normal tissue were used to test VEGF receptor Ⅱ and CD34 expression level and ERK 1/2 activity level. RESULTS: ERK 1/2 activity level from the first to the 4th day,VEGF receptor Ⅱ and CD34 expression level from the 4th to the 14th day after the operation,were all higher in the Rhodiolae group than that in the saline group. CONCLUSION: Rhodiolae rosae can elevate ERK 1/2 activity which was related to and prior to its angiogenic effect.
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Objective: To investigate the effect of Shexiangbaoxin Pills on morphosis and function of left ventricle after myocardial infarction in rat. Methods: The rat myocardial infarction models induced by ligaturing coronary artery were randomly divided into the myocardial infarction control group, Shexiangbaoxin Pill group and captopril group. The hemodynamic parameters and cardiac functions in 2 or 6 weeks after treatment were determined. Meantime, the morphological parameters of left ventrile (left cardiac chamber size, attenuation proportion of ventricular wall of infarction area, and expansion index of left ventrile), were studied. Results: Shexiangbaoxin Pills could reduce the distention of left ventrile and expansion of infarction area of rat in 6 weeks after infarction. It could obviously improve the contraction function of left ventrile after myocardial infarction. Conclusion: Shexiangbaoxin Pills can improve left ventricular reconstitution after myocardial infarction.
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Objective:The stimulate angiogenes effect and mechanism of Shexiangbaoxin Pills on coronary collateral development in the hearts of experimental myocardial infarction rats were studied. Methods:24 myocardial infarction rats were randomly divided into 3 groups, 8 rats in group A were treated with Shexiangbaoxin Pills, 8 rats in group B were treated with Beifuji and heparin, and 8 rats in group C were treated with 0.9% normal saline as control. Infarct area, the contents of VEGF、bFGF and VⅢ factor, and vascular density in the edge of infarct section were measured after 6 weeks treating.Results: Infarct area in group A was obviously less than that in group C, the contents of VEGF、bFGF and VⅢ factor in the edge of infarct section and vascular density in group were significantly increased compared with those in group C. Conclusions: Shexiangbaoxin Pills could stimulate angiogenesis of the collateral branch of coronary artery in ischemic myocardium of rats and showed good protective on myocardial ischemia.
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AIM: The effect of decreasing infarct area and stimulating angiogenesis of Shexiangbaoxin Pills in rat with coronary occlusion were studied. METHODS: 44 rats with ligation of the left coronary artery were randomly divided into 4 roups:11 rats were treated with small dose Shexiangbaoxin Pills (group 1), 11 rats were treated with high dose Shexiangbaoxin Pills (group 2), 11 rats were treated with Beifuji and heparin (group 3), 11 rats were treated with 0.9% normal saline (group 4). 18 rats were randomly divided into 2 control groups:10 sham operated rats (group 5) and 8 normal rats (group 6). Infarct area and vascular density in the edge of infarct section were measured after treating for 8 weeks. RESULTS: Infarct area in group 1,2 and 3 was obviously less than that in group 4. The difference was not significant between group 1 and group 3 but group 2 was better than group 3. The difference was significant between group 1 and group 2. The vascular density in group 1,2 and 3 were significanly increased in comparison with those in group 4. The difference was not significant between group 2 with 3. CONCLUSION: Shexiangbaoxin Pills could decrease infarct area and stimulate angiogenesis of the experimental myocardial infarction rat. The effect of Shexiangbaoxin Pills was equal to the group treated with Beifuji and heparin. Shexiangbaoxin Pills had a dose response relationship.
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AIM: We observed the expression of KDR/Flk1 in post-myocardiac ischemia(MI) SD rats in order to explain the effect of captopril and its relationship with myocardium angiogenesis after long-term administration.METHODS: The MI model was made by LAD ligation.Captopril was administered for 6 weeks.Immuohistological method and FQ-PCR were used to test the myocardium KDR/Flk-1 expression.RESULTS: In captopril group,no inhibitory effect was observed in myocardium factor VIII expression,but KDR/Flk-1 decreased.The copies of KDR/Flk-1 mRNA reduced dramatically when compared to control group,false-operation and normal group(P0.05).CONCLUSION: ACEI down-regulates KDR/Flk-1 and its mRNA expression in ischemic rat myocardium after long-term administration of captopril,but does not inhibit angiogenesis.So we suspect that some other pathways exist,which can not affect by ACEI,or that ACEI just reduces abnormal angiogenesis.