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Objective:To observe the protective effect and mechanism of combination of puerarin combined with tanshinone ⅡA on diabetes mellitus (DM) rats with vascular lesions. Method:The SD rats (fed with high-fat diet) were administrated with streptozotocin(STZ) through intravenous injection to make the model of diabetic vascular lesions. The successfully modeled rats were randomly divided into the model control group, the high-dose group (0.5 g·kg-1+1.0 g·kg-1), the middle-dose group (0.25 g·kg-1+0.5 g·kg-1), the low-dose group (0.05 g·kg-1+0.1 g·kg-1), the puerarin group (0.25 g·kg-1), the tanshinone ⅡA group (0.5 g·kg-1) and the positive control group (Metformin, 0.09 g·kg-1). Each group was administrated with drugs respectively by gavage for 70 days. After intervention in each group, the general conditions and body weight of the rats were observed. The contents of blood grucose and blood lipids were determined by automatic biochemical analyzer. The contents of insulin, advanced glycation end products (AGEs), superoxide dismutase(SOD), glutathione peroxidase (GSH-Px) in serum, the contents of tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and thromboxane B2 (TXB2) in plasma, as well as the contents of AGEs and oxidized low-density lipoprotein(ox-LDL) in aorta homogenate were detected by enzyme-linked immunosorbent assay(ELISA). The content of malondialdehyde(MDA) in serum was determined by chemical colorimetry. Pathological changes of coronary tissue were observed by htoxylin eosin(HE) staining. The expression of PAI-1 protein of aorta was observed by immunohistochemistry. Result:Compared with the normal control group, in the model group, the levels of blood grucose and blood lipids (PPPP2 in plasma (PPPPPPPPP2 in plasma (PPPPPPPConclusion:Puerarin combined with Tanshinone ⅡA could relieve vascular lesions of DM rats. The mechanisms may be related to the reduction of oxidative stress and the regulation of coagulation-fibrinolysis system.
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Objective To investigate the effect of polymorphism of plasminogen activator inhibitor-1(PAI-1) promotor region gene,plasma tissue plasminogen activator(t-PA)and PAI-1 on patients with acute pulmonary thromboembolism(APTE).Method Fifty-two patients with APTE were divided into two groups according to the presence or absence of traditional enviromnent risk facters,and there were26 patients in each gnup,and auother 57 healthy indiriduals as controls were analyzed.The genotypos of subjects were determined for the 4G/5G polymorphism of PAI-1 gene using polymerase chain reaction based restriction fragment length polymorphism analysis.Plasma PAI-1 and tPA were measured by ELISA.Results(1)The ratio of 4G/4G genotype in group without traditional environment risk factors was much higher than that of the other two groups.(2)Plasma t-PA decreased and plasma PAI-1 elevated significantly in group without traditional environment risk factors compared with that of the other two groups.(3)Except the 5G homozygous,plasma PAI-1 level in group without traditional environgment risk factors was significantly higher than the other two groups.There existed correlation between 4G allele and plasma PAI-1.Conclusions 4G/5G polymorphism of PAI-1 gene is associated with AFFE.4G/4G genotype increases the risk of APTE for individuals without traditional risk factors.There are hypercoagulation and hypofibrinolysis in APTE patients without traditional risk factors.
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Effects of 38°C 30-minute bathing on hemostatic function and autonomic nervous function were studied in 15 48-to-72-year-old patients with cerebral infarction. Blood samples were collected three times: immediately before the bathing, at the end of 30 minutes of bathing, and 30 minutes after the bathing. Hematocrit values and fibrinogen concentrations decreased during bathing and returned to the pre-bathing levels 30 minutes after bathing. This indicates that bathing caused hemodilution due to the fluid shift. During bathing, noradrenaline decreased at a rate significantly higher than that of hemodilution while the sympathetic nervous function, which was evaluated by spectral analysis of sequential variation in arterial blood pressure, was not suppressed. The autonomic nervous system seemed to be inactive in these patients. Coagulation time (PT and APTT) and platelet factor (β-TG and PF4) showed few changes. In the fibrinolytic system, however, tissue plasminogen activator (t-PA) antigen levels increased and plasminogen activator inhibitor type-1 (PAI-1) levels decreased after 30 minutes of bathing. This suggests that fibrinolytic activity was enhanced by 38°C bathing for 30 minutes. Thus, subthermal bathing with comfort may be useful in preventing cerebral infarction.
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Studies on the effects of heating as well as the mineral components of hot spring water have been conducted to investigate the effects of balneotherapy. However, few studies have been conducted on the effects of hydrostatic pressure and buoyancy during water immersion. Therefore, we investigated the effect of water immersion up to the neck at thermoneutral temperature on hemostatic activity.<br>Nine healthy men aged 22 to 34 were immersed up to the neck in the standing position in thermoneutral water (34.0±0.5°C) for two hours. The heart rate decreased immediately after starting water immersion and remained low during the immersion. Hematocrit values (Ht) of the blood samples taken from the ante-cubital vein decreased by 3.4% in average. The decrease in Ht was more prominent in the blood samples taken from the earlobe (4.0%), suggesting that hemodilution due to fluid shift was stronger in the upper part of the body. The time until euglobulin clot lysis shortened immediately after starting the immersion. Although fibrinolytic activity was enhanced, the concentration of tissue plasminogen activator (t-PA) antigen in the blood decreased gradually during the immersion and tended to return to the original level 30 minutes after immersion. A larger decrease in the concentration of plasminogen activator inhibitor-1 (PAI-1) antigen in the blood was observed immediately after starting the immersion, and it remained low for 30 minutes after immersion. An increase in fibrinolytic activity due to the decrease in PAI-1, not in t-PA, was observed during water immersion at thermoneutral temperature and the activation of fibrinolytic system without activation of the coaguration system was also observed.
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BACKGROUND: It is well known that coronary arterial thrombosis plays an important role in the pathogenesis of acute coronary syndrome and this has focused interest on the role of the fibrinolytic system, especially tissue plasminogen activator(t-PA) and plasminogen activator inhibitor-1(PAI-1), which are major determinants of fibrinolytic system. But there are considerable variations in the reported association between these two components and acute coronary syndrome. METHODS: To evaluate association between t-PA, PAI-1 and myocardial infarction, plasma level of t-PA and PAI-1 in resting state and after venous occlusion were measured and analysed in patients with previous myocardial infarction at least 6 months after the acute phase, who showed less than 70% luminal narrowing angiographically and control group. The relationship between t-PA, PAI-1 antigen and activity and relation to age, serum triglyceride, cholesterol, and peak creatine kinase(CK) enzyme were also analyzed. RESULTS: 1) In resting state, there was a significant difference of plasma level of both t-PA and PAI-1 antigen, activity between patient and control group(10.72+/-3.28 vs 8.16+/-4.03ng/ml, 0.53+/-0.34 vs 0.02+/-0.07U/ml, 26.24+/-8.30 vs 20.82+/-8.82ng/ml, 14.62+/-5.97 vs 6.99+/-6.44U/ml)(p<0.05), and resting plasma level of PAI-1 activity showed a good correlation with peak creatine kinase(CK) enzyme(r=0.76, p<0.01). 2) After venous occlusion, plasma level of t-PA antigen was significantly increased(8.16+/-4.03 vs 9.87+/-3.86ng/ml)(p<0.05) whereas t-PA activity and PAI-1 antigen were not significantly changed in control group. In patient group, t-PA antigen, t-PA activity and PAI-1 antigen were significantly inceased after venous occlusion(10.72+/-3.28 vs 14.66+/-5.41ng/ml, 0.53+/-0.34 vs 1.41+/-1.69U/ml, 26.24+/-8.30 vs 29.87+/-8.78ng/ml)(p<0.05). PAI-1 activity was significantly decreased after venous occlusion in both groups(6.99+/-6.44 vs 6.06+/-5.99U/ml, 14.62+/-5.97 vs 12.67+/-6.46U/ml)(p<0.05). CONCLUSION: Both fibrinolytic and anti-fibrinolytic systems are augmented in resting and after fibrinolysis stimulation test in patient group. These findings suggested a impairment of fibrinolytic system in patient group and a possibility that both elevated plasma levels of t-PA and PAI-1 may be markers of coronary artery disease.
Subject(s)
Humans , Acute Coronary Syndrome , Cholesterol , Coronary Artery Disease , Creatine , Fibrinolysis , Myocardial Infarction , Phenobarbital , Plasma , Plasminogen Activator Inhibitor 1 , Plasminogen Activators , Plasminogen , Thrombosis , Tissue Plasminogen Activator , TriglyceridesABSTRACT
Objective: To investigate the effect of leech injection on thrombosis and plasma tissue plasminogen activator (t PA) and its inhibitor (PAI) in the thrombosis model of mice. Methods: The different dose leech injection of different doses were given to mice in different groups for 7 days respectively. Thrombosis was induced in mice by carrageenan. The plasma t PA and PAI activity were detected by chromogennic substracte analysis.Results: The average thrombosis length of tail in the groups of leech injection were significantly shorter than the length in the groups of thrombosis control. Compared with the group of thrombosis control, the plasma PAI activity in the leech injection groups was lower. Conclusions: The leech injection can reduce thrombosis in mice. The mechanism might be associated with reducing the release of PAI.