本文選題：空氣污染 + 細顆粒物　； 參考：《第三軍醫(yī)大學(xué)學(xué)報》2016年04期

【摘要】：目的探討父代大鼠長期暴露大氣細顆粒物(fine particulate matter,PM2.5)對其子代血壓及尿鈉排泄的影響。方法將20只8~10周齡,體質(zhì)量180~200 g的雄性SD(Sprague-Dawley)大鼠采用完全隨機方法分為暴露組和對照組(n=10)。暴露組經(jīng)氣道滴灌PM2.5混懸液(10 mg/m L,20μL/次,2次/周,共12周),對照組同法滴灌等量PBS緩沖液。12周后與健康雌性SD大鼠交配分別得到暴露組子代和對照組子代。標準飼料喂養(yǎng)子代大鼠至7~8周齡,體質(zhì)量180~200 g,用無創(chuàng)鼠尾血壓監(jiān)測儀測定2組子代大鼠血壓,代謝籠法收集24 h尿液并測定尿量、尿鈉排泄情況,通過腎上腺動脈灌注多巴胺受體激動劑非諾多泮觀察腎臟利尿排鈉功能,Western blot檢測子代大鼠腎臟組織G蛋白偶聯(lián)受體激酶4(G protein coupled receptor kinase 4,GRK4)、多巴胺Ⅰ類受體(D1DR)蛋白表達情況。結(jié)果與對照組子代相比,暴露組子代血壓明顯升高[(130.2±2.6)vs(113.0±0.5),P0.05];D1受體介導(dǎo)的利尿排鈉功能受損[尿流速:(7.52±1.98)vs(10.71±2.05),P0.05;尿鈉排泄率:(522.8±211.1)vs(990.6±231.0),P0.05];子代大鼠腎臟GRK4蛋白水平明顯增加[(0.81±0.06)vs(0.67±0.09),P0.05],D1受體蛋白表達降低[(0.53±0.05)vs(0.64±0.04)]。結(jié)論父代大鼠長期暴露PM2.5會引起其子代大鼠成年時期血壓升高,可能與PM2.5影響子代腎臟GRK4的表達從而引起D1受體介導(dǎo)的利尿排鈉功能障礙相關(guān)。
[Abstract]:Objective to investigate the long-term exposure of parent rats of atmospheric fine particles (fine particulate matter, PM2.5) effects on the offspring blood pressure and urinary sodium excretion. Methods 20 8~10 weeks of age, body mass of 180~200 g SD (Sprague-Dawley) male rats were randomly divided into the method of exposure group and the control group (n=10). The exposure group by airway drip irrigation PM2.5 suspension (10 mg/m L, 20 L/, 2 times / week, for 12 weeks), the control group with the same amount of PBS buffer drip after.12 weeks and healthy female SD rats were mated respectively exposed offspring and control group standard diet progeny. Feeding rat offspring to 7~8 weeks old, weighing 180~200 g, rat tail blood pressure monitor to measure the blood pressure of 2 groups of rat offspring with noninvasive, metabolic cage method to collect 24 h urine and urinary volume, urinary sodium excretion, the adrenal artery infusion of dopamine receptor agonist fenoldopam on kidney diuresis sodium excretion function, Western Blot detection of renal tissue of rat G protein coupled receptor kinase 4 (G protein coupled receptor kinase 4, GRK4), dopamine receptor type 1 (D1DR) protein expression. Results compared with the control group offspring exposed offspring significantly increased blood pressure [(130.2 + 2.6) vs (113 + 0.5). P0.05]; D1 receptor-mediated natriuretic dysfunction [: urinary flow rate (7.52 + 1.98) vs (10.71 + 2.05), P0.05; urinary sodium excretion rate (522.8 + 211.1) vs (990.6 + 231), P0.05]; offspring rat kidney GRK4 protein level increased [(0.81 + 0.06 VS) (0.67 + 0.09), P0.05], expression of D1 protein decreased [(0.53 + 0.05) vs (0.64 + 0.04). Conclusion the parent rats exposure to PM2.5 can cause the adult rat offspring period of elevated blood pressure, and PM2.5 may affect the expression of offspring of renal GRK4 causing D1 receptor mediated the urinary sodium excretion function.

【作者單位】： 第三軍醫(yī)大學(xué)大坪醫(yī)院野戰(zhàn)外科研究所心血管內(nèi)科 重慶市心血管病研究所;
【基金】：國家重點基礎(chǔ)研究發(fā)展計劃(973計劃,2012CB517801)~~
【分類號】：R122
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本文編號：1756331