大氣中硫化合物對腦卒中急診及SD大鼠血壓調控的影響
發(fā)布時間：2018-09-08 16:54
【摘要】：目的： 1.研究氣態(tài)硫化合物二氧化硫(SO2)對腦卒中急診影響及季節(jié)性差異。 2.探討顆粒硫化合物硫酸鉛對人臍靜脈內皮細胞(HUVEC)活力、RAS系統(tǒng)的影響。 3.闡明顆粒硫化合物硫酸鉛對SD大鼠血壓及RAS系統(tǒng)的影響及ACEI在其中的調控作用。 方法： 1.收集2008-2009年長沙市湘雅三醫(yī)院每日腦卒中急診數(shù)據(jù)及相關氣象和大氣污染數(shù)據(jù),運用單向回顧性1：4病例交叉設計,分析不同季節(jié)S02對腦卒中急診事件的影響。 2.將人臍靜脈內皮細胞(HUVEC)分為對照組和實驗組,依據(jù)大氣細顆粒(PM2.5)中鉛的含量(0.042%),結合文獻設計低(0.17μg/ml)、中(0.85μg/ml)、高(4.25μg/ml)濃度硫酸鉛干預HUVEC24h。MTT法檢測細胞活力改變,普通逆轉錄PCR、western blot、ELISA檢測ACE、AngII、AT1R mRNA及蛋白表達的變化。 3.24只SD大鼠隨機分為對照組、硫酸鉛干預組、硫酸鉛+卡托普利組和卡托普利組。硫酸鉛+卡托普利組及卡托普利組予以卡托普利灌胃3d (100mg/(kg. d)),其他兩組予以灌胃相應劑量生理鹽水；3d后,硫酸鉛干預組及硫酸鉛+卡托普利組予以氣管滴注硫酸鉛(84μg/kg),余兩組滴注相應劑量生理鹽水。染毒1d后檢測大鼠血壓變化,ELISA檢測大鼠腹主動脈血AngII、Ang (1-7)變化,普通逆轉錄PCR和western blot檢測大鼠心肌和胸主動脈ACE、AT1R、ACE2. Mas mRNA和蛋白的改變。 結果： 1.在調整氣象因素(氣溫和相對濕度)的單污染物滯后模型中,秋季滯后0-3d的SO2日均濃度每增加10μ g/m3,總腦卒中及腦出血和腦梗死亞型急診OR值均大于1,且關聯(lián)具有統(tǒng)計學意義(P(0.05)；在同時控制NO2和PM10的多污染物模型中,秋季SO2濃度每增加10μ g/m3時,總腦卒中和腦梗死急診的OR值(95%CI)為1.301(95%CI:1.038-1.631)、1.446(95%CI:1.130-1.850)(P0.05)。 2.HUVEC細胞暴露于低、中、高濃度硫酸鉛24h后,各組HUVEC細胞存活率較對照組均下降,但差異無統(tǒng)計學意義(P0.05)；各組ACE、及AT1R mRNA表達較對照組均升高,中、高濃度組與對照組差異有統(tǒng)計學意義(P0.05)；各組AT1R、AngII蛋白表達較對照組升高,中、高濃度組與對照組差異有統(tǒng)計學意義(P0.05)；中、高濃度組ACE蛋白表達較對照組升高,高濃度組與對照組差異有統(tǒng)計學意義(P0.05)。 3.硫酸鉛染毒后大鼠收縮壓及舒張壓均有所增加,其中舒張壓較對照組差異有統(tǒng)計學意義(P0.05),卡托普利預處理后可以顯著減弱硫酸鉛成分對大鼠舒張壓的影響(P0.05)；同時大鼠血漿AngII水平及心肌、主動脈ACE、AT1R蛋白表達較對照組顯著升高(P0.05),但對大鼠血漿Ang(1-7)、心肌及主動脈ACE2及Mas受體的影響無統(tǒng)計學意義(P0.05)；卡托普利預處理可以顯著減弱硫酸鉛對大鼠血漿AngII、心肌、主動脈ACE及AT1R的影響(P0.05)。 結論： 1.研究區(qū)域秋季SO2日均濃度增加,導致腦卒中急診事件增多,對腦梗死急診事件影響更為顯著。 2.硫酸鉛可上調內皮細胞ACE-AngII-AT1R軸mRNA和蛋白質表達。 3.硫酸鉛急性暴露引起大鼠舒張壓顯著增高,同時激活大鼠心肌及主動脈ACE-AngII-AT1R軸蛋白表達,ACEI可降低硫酸鉛導致的血壓增高及ACE-AngII-AT1R軸蛋白的過度激活。
[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.
【學位授予單位】：中南大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：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.
【學位授予單位】：中南大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R743.3
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