摘要: | 粒子直徑小於2.5微米的懸浮粒子(PM2.5),可經人體呼吸到達支氣管與肺泡中,並累積於肺臟中,其總比表面積大於PM10,體積更小於PM10使其更易吸附有毒害的相關物質,甚至干擾肺部氣體交換,但至目前為止PM2.5對於心臟的影響及其作用機制仍不清楚。
我們的研究表明,(1)小鼠暴露於PM2.5會引起血壓升高(收縮壓增加1.5倍、舒張壓增加1.7倍)、心臟電訊號異常(QT間期延長2.3倍、動作電位平台期延長4.9倍),並造成心臟結構的改變(造成15%的心臟肥大與35%的纖維化);(2)餵食褐藻醣膠後,對於血壓升高、心臟電訊號異常及其結構改變具改善效果。其中收縮壓降低20%、舒張壓降低30%、QT間期延長縮短60%、動作電位平台期延長減少70%,心臟肥大的程度由15%降為8%、纖維化程度則;由35%減為15%;(3)餵食褐藻醣膠後,影響心臟電訊號異常、結構改變的相關基因,其表現量均有減少的趨勢;(4) PM2.5中所含的有機及無機重金屬成分,確實會殘留在小鼠體內,經餵食褐藻醣膠後其累積量明顯減少。以鎘(Cd)、砷(As)、鉛(Pb)、銅(Cu)及汞(Hg)為例,除Hg無顯著影響外,在血液內殘留量分別減少90% Cd、70% As、30% Pb及70% Cu,而在其他臟器(心臟、肝臟、肺臟、腎臟)中亦有相同的趨勢,證明褐藻醣膠確實有改善的作用。
根據我們的實驗結果,顯示PM2.5確實會造成心臟的異常,且證明褐藻醣膠能夠改善因暴露於PM2.5引起的血壓升高、心臟電訊號功能異常及其結構改變,故可將褐藻醣膠視極為具有優勢的保健食品。另外可利用因暴露於PM2.5產生之高血壓鼠建立模式小鼠研究平台進行高血壓之相關研究。
Suspended particulates in the atmosphere are complex particulate matter, the main source of particulate matter are haze on the surface, dust, dust storms, burning energy, minerals, second-hand smoke and volcanic eruptions. The particle diameter less than 10μm suspended particles is called PM10, can reach through the human respiratory system and accumulate in lung. In addition, suspended particles of less than 2.5μm (PM2.5), which surface area is greater and volume is less than PM10, make it easier to adsorb toxic substance, and interfere with pulmonary gas exchange.
Our results indicated that: 1) PM2.5 exposure caused blood pressure increase, abnormal cardiac electrophysiologies (prolongation of QT interval and action potential platform stage), and structral remodeling (cardiac hypertrophy and fibrosis); 2) Fucoidan supplement can rescue these PM2.5-induced myocardial injury; 3) We also focused on the mechanism, expression of genes related to abnormal cardiac electrophysiologies and structral remodeling decreased after feeding fucoidan; 4) Organic and inorganic compounds in PM2.5 decreased after feeding fucoidan in mice blood and organs.
According to the results from my experiments, after feeding fucoidan, high blood pressure, abnormal cardiac electrophysiologies, hypertrophy, and fibrosis caused by PM2.5 in heart can be rescued. Besides, we can design some further studies based on our PM2.5-induced high blood pressure mice. |