大气中硫化合物对脑卒中急诊及SD大鼠血压调控的影响
发布时间：2018-09-08 16:54
【摘要】：目的： 1.研究气态硫化合物二氧化硫(SO2)对脑卒中急诊影响及季节性差异。 2.探讨颗粒硫化合物硫酸铅对人脐静脉内皮细胞(HUVEC)活力、RAS系统的影响。 3.阐明颗粒硫化合物硫酸铅对SD大鼠血压及RAS系统的影响及ACEI在其中的调控作用。 方法： 1.收集2008-2009年长沙市湘雅三医院每日脑卒中急诊数据及相关气象和大气污染数据,运用单向回顾性1：4病例交叉设计,分析不同季节S02对脑卒中急诊事件的影响。 2.将人脐静脉内皮细胞(HUVEC)分为对照组和实验组,依据大气细颗粒(PM2.5)中铅的含量(0.042%),结合文献设计低(0.17μg/ml)、中(0.85μg/ml)、高(4.25μg/ml)浓度硫酸铅干预HUVEC24h。MTT法检测细胞活力改变,普通逆转录PCR、western blot、ELISA检测ACE、AngII、AT1R mRNA及蛋白表达的变化。 3.24只SD大鼠随机分为对照组、硫酸铅干预组、硫酸铅+卡托普利组和卡托普利组。硫酸铅+卡托普利组及卡托普利组予以卡托普利灌胃3d (100mg/(kg. d)),其他两组予以灌胃相应剂量生理盐水；3d后,硫酸铅干预组及硫酸铅+卡托普利组予以气管滴注硫酸铅(84μg/kg),余两组滴注相应剂量生理盐水。染毒1d后检测大鼠血压变化,ELISA检测大鼠腹主动脉血AngII、Ang (1-7)变化,普通逆转录PCR和western blot检测大鼠心肌和胸主动脉ACE、AT1R、ACE2. Mas mRNA和蛋白的改变。 结果： 1.在调整气象因素(气温和相对湿度)的单污染物滞后模型中,秋季滞后0-3d的SO2日均浓度每增加10μ g/m3,总脑卒中及脑出血和脑梗死亚型急诊OR值均大于1,且关联具有统计学意义(P(0.05)；在同时控制NO2和PM10的多污染物模型中,秋季SO2浓度每增加10μ g/m3时,总脑卒中和脑梗死急诊的OR值(95%CI)为1.301(95%CI:1.038-1.631)、1.446(95%CI:1.130-1.850)(P0.05)。 2.HUVEC细胞暴露于低、中、高浓度硫酸铅24h后,各组HUVEC细胞存活率较对照组均下降,但差异无统计学意义(P0.05)；各组ACE、及AT1R mRNA表达较对照组均升高,中、高浓度组与对照组差异有统计学意义(P0.05)；各组AT1R、AngII蛋白表达较对照组升高,中、高浓度组与对照组差异有统计学意义(P0.05)；中、高浓度组ACE蛋白表达较对照组升高,高浓度组与对照组差异有统计学意义(P0.05)。 3.硫酸铅染毒后大鼠收缩压及舒张压均有所增加,其中舒张压较对照组差异有统计学意义(P0.05),卡托普利预处理后可以显著减弱硫酸铅成分对大鼠舒张压的影响(P0.05)；同时大鼠血浆AngII水平及心肌、主动脉ACE、AT1R蛋白表达较对照组显著升高(P0.05),但对大鼠血浆Ang(1-7)、心肌及主动脉ACE2及Mas受体的影响无统计学意义(P0.05)；卡托普利预处理可以显著减弱硫酸铅对大鼠血浆AngII、心肌、主动脉ACE及AT1R的影响(P0.05)。 结论： 1.研究区域秋季SO2日均浓度增加,导致脑卒中急诊事件增多,对脑梗死急诊事件影响更为显著。 2.硫酸铅可上调内皮细胞ACE-AngII-AT1R轴mRNA和蛋白质表达。 3.硫酸铅急性暴露引起大鼠舒张压显著增高,同时激活大鼠心肌及主动脉ACE-AngII-AT1R轴蛋白表达,ACEI可降低硫酸铅导致的血压增高及ACE-AngII-AT1R轴蛋白的过度激活。
[Abstract]:Objective:
1. to study the effects of gaseous sulfur compounds sulfur dioxide (SO2) on stroke emergency and seasonal differences.
2. to investigate the effect of lead sulfate on human umbilical vein endothelial cells (HUVEC) and RAS system.
3. To clarify the effect of granular lead sulfate on blood pressure and RAS system in SD rats and the regulation of ACEI.
Method:
1. Daily emergency data of stroke and related meteorological and atmospheric pollution data of Changsha Xiangya Third Hospital from 2008 to 2009 were collected. The effects of S02 on emergency events of stroke in different seasons were analyzed by one-way retrospective 1:4 case crossover design.
2. Human umbilical vein endothelial cells (HUVEC) were divided into control group and experimental group. According to the content of lead in PM2.5 (0.042%), low (0.17 ug/ml), medium (0.85 ug/ml) and high (4.25 ug/ml) concentration of lead sulfate were designed to interfere with HUVEC 24 h. MTT assay was used to detect the changes of cell viability. Changes of mRNA and protein expression.
3.24 SD rats were randomly divided into control group, lead sulfate intervention group, lead sulfate + captopril group and captopril group. The blood pressure of rats was measured one day after exposure. AngII and Ang (1-7) in abdominal aorta blood were detected by ELISA. ACE, AT1R, ACE2.Mas mRNA and protein in myocardium and thoracic aorta were detected by RT-PCR and Western blot.
Result:
1. In the single pollutant hysteresis model with adjusted meteorological factors (air temperature and relative humidity), the OR values of total stroke, cerebral hemorrhage and cerebral infarction subtypes were higher than 1 for each increase of 10 ug/m3 of SO2 concentration per day with 0-3 days lag in autumn, and the correlation was statistically significant (P (0.05); in the multi-pollutant model with simultaneous control of NO2 and PM 10, the concentration of SO2 in autumn was higher than 1. The OR values of total stroke and cerebral infarction emergency (95% CI) were 1.301 (95% CI: 1.038-1.631) and 1.446 (95% CI: 1.130-1.850) (P 0.05).
2. HUVEC cells exposed to low, medium and high concentrations of lead sulfate 24 hours later, the survival rate of HUVEC cells in each group decreased, but the difference was not statistically significant (P 0.05); ACE, and AT1R mRNA expression in each group were higher than that in the control group, the difference was statistically significant (P 0.05); AT1R, AngII protein expression in each group was higher than that in the control group. The expression of ACE protein in high concentration group was significantly higher than that in control group (P 0.05).
3. The systolic and diastolic blood pressures of rats exposed to lead sulfate were increased, and the diastolic blood pressure was significantly higher than that of the control group (P There was no significant difference in plasma Ang (1-7), myocardial and aortic ACE2 and Mas receptors (P 0.05). Captopril pretreatment could significantly attenuate the effects of lead sulfate on plasma AngII, myocardial, aortic ACE and AT1R (P 0.05).
Conclusion:
1. The increase of SO2 concentration in the study area in autumn led to the increase of stroke emergency events, and the impact on cerebral infarction emergency events was more significant.
2. lead sulfate can increase the expression of mRNA and protein in ACE-AngII-AT1R axis of endothelial cells.
3. Acute exposure to lead sulfate can increase diastolic blood pressure and activate ACE-AngII-AT1R axon protein expression in myocardium and aorta of rats. ACEI can decrease lead sulfate-induced hypertension and ACE-AngII-AT1R axon overactivation.
【学位授予单位】：中南大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R743.3
[Abstract]:Objective:
1. to study the effects of gaseous sulfur compounds sulfur dioxide (SO2) on stroke emergency and seasonal differences.
2. to investigate the effect of lead sulfate on human umbilical vein endothelial cells (HUVEC) and RAS system.
3. To clarify the effect of granular lead sulfate on blood pressure and RAS system in SD rats and the regulation of ACEI.
Method:
1. Daily emergency data of stroke and related meteorological and atmospheric pollution data of Changsha Xiangya Third Hospital from 2008 to 2009 were collected. The effects of S02 on emergency events of stroke in different seasons were analyzed by one-way retrospective 1:4 case crossover design.
2. Human umbilical vein endothelial cells (HUVEC) were divided into control group and experimental group. According to the content of lead in PM2.5 (0.042%), low (0.17 ug/ml), medium (0.85 ug/ml) and high (4.25 ug/ml) concentration of lead sulfate were designed to interfere with HUVEC 24 h. MTT assay was used to detect the changes of cell viability. Changes of mRNA and protein expression.
3.24 SD rats were randomly divided into control group, lead sulfate intervention group, lead sulfate + captopril group and captopril group. The blood pressure of rats was measured one day after exposure. AngII and Ang (1-7) in abdominal aorta blood were detected by ELISA. ACE, AT1R, ACE2.Mas mRNA and protein in myocardium and thoracic aorta were detected by RT-PCR and Western blot.
Result:
1. In the single pollutant hysteresis model with adjusted meteorological factors (air temperature and relative humidity), the OR values of total stroke, cerebral hemorrhage and cerebral infarction subtypes were higher than 1 for each increase of 10 ug/m3 of SO2 concentration per day with 0-3 days lag in autumn, and the correlation was statistically significant (P (0.05); in the multi-pollutant model with simultaneous control of NO2 and PM 10, the concentration of SO2 in autumn was higher than 1. The OR values of total stroke and cerebral infarction emergency (95% CI) were 1.301 (95% CI: 1.038-1.631) and 1.446 (95% CI: 1.130-1.850) (P 0.05).
2. HUVEC cells exposed to low, medium and high concentrations of lead sulfate 24 hours later, the survival rate of HUVEC cells in each group decreased, but the difference was not statistically significant (P 0.05); ACE, and AT1R mRNA expression in each group were higher than that in the control group, the difference was statistically significant (P 0.05); AT1R, AngII protein expression in each group was higher than that in the control group. The expression of ACE protein in high concentration group was significantly higher than that in control group (P 0.05).
3. The systolic and diastolic blood pressures of rats exposed to lead sulfate were increased, and the diastolic blood pressure was significantly higher than that of the control group (P There was no significant difference in plasma Ang (1-7), myocardial and aortic ACE2 and Mas receptors (P 0.05). Captopril pretreatment could significantly attenuate the effects of lead sulfate on plasma AngII, myocardial, aortic ACE and AT1R (P 0.05).
Conclusion:
1. The increase of SO2 concentration in the study area in autumn led to the increase of stroke emergency events, and the impact on cerebral infarction emergency events was more significant.
2. lead sulfate can increase the expression of mRNA and protein in ACE-AngII-AT1R axis of endothelial cells.
3. Acute exposure to lead sulfate can increase diastolic blood pressure and activate ACE-AngII-AT1R axon protein expression in myocardium and aorta of rats. ACEI can decrease lead sulfate-induced hypertension and ACE-AngII-AT1R axon overactivation.
【学位授予单位】：中南大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R743.3
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