DEHP致小鼠哮喘和氧化应激关系的初步研究

发布时间：2018-11-18 16:13

【摘要】：DEHP是一种人工合成的化学物质,常作为增塑剂添加到塑料制品中,用以增加塑料制品的柔韧性。DEHP的物理性质为无色也基本无味,不易蒸发。随着工业的发展,邻苯二甲酸酯类物质比上个世纪更密切的贴近我们的生活之中,无论是居住环境还是食品、饮用品,乃至医疗用品中我们都接触着形形色色的邻苯二甲酸酯类物质。而氧化应激反应是一个在机体普遍发生的应激反应,它形成的原因多种多样,它表现的形式千变万化,近几年逐渐成为了热门话题。在之前的研究中我们已经知道DEHP在小鼠的过敏性哮喘中起到的是佐剂作用。而DEHP也能引起氧化应激反应的发生,氧化应激是否也是DEHP导致小鼠过敏性哮喘的途径现在还没有明确的定论。本论文的研究中,实验分为两个大组,即生理盐水对照的非致敏组和OVA对照的致敏组。其中,生理盐水对照的非致敏组又分为生理盐水对照组,DEHP染毒组和维生素E单独作用组；OVA对照的致敏组分为OVA单独致敏组,DEHP染毒OVA致敏组,DEHP和维生素E联合作用OVA致敏组,维生素E单独作用OVA致敏组,共7个实验组。整个实验周期共18天,其中DEHP染毒和维生素E作用的时间为14天,致敏组在第1天和第11天用OVA致敏(非致敏组注射生理盐水),雾化激发期为4天。上午进行DEHP灌胃染毒,下午进行维生素E灌胃修复。全天两次灌胃后进行喂食。本实验中DEHP染毒浓度为30mg/kg·d,维生素E修复浓度亦为30mg/kg·d,对照组用生理盐水灌胃。OVA致敏采用83.33μgOVA和292mgAl(OH)3的混合液500μL对小鼠腹腔注射和皮下注射混合致敏,其中200μL腹腔注射,300μL皮下多点注射(每次5点)。雾化激发则为含1%OVA的生理盐水溶液连续雾化30min。建模后测量ROS, GSH, IL-4, IgE等生理生化指标。实验结果说明：氧化应激反应与小鼠过敏性哮喘的发生有相关性。氧化应激反应加重时小鼠过敏性哮喘程度增加,加入抗氧化剂保护后的小鼠的过敏性哮喘程度下降。说明氧化应激是DEHP导致小鼠过敏性哮喘的有效途径。
[Abstract]:DEHP is a synthetic chemical substance, which is often added to plastic products as plasticizer to increase the flexibility of plastic products. The physical properties of DEHP are colorless and basically tasteless, so it is not easy to evaporate. With the development of industry, phthalates are closer to our daily life than in the last century, whether it is living environment or food, drinking articles, Even in medical supplies we are exposed to all kinds of phthalates. The oxidative stress reaction is a common stress reaction in the body, it is formed for a variety of reasons, its performance of a variety of forms, in recent years has become a hot topic. In previous studies we have known that DEHP acts as an adjuvant in allergic asthma in mice. However, DEHP can also induce oxidative stress. Whether oxidative stress is the pathway of allergic asthma induced by DEHP in mice is not clear. In the present study, the experiment was divided into two groups: the non-sensitized group with normal saline control and the sensitized group with OVA control. Among them, the non-sensitized group of normal saline control group was divided into normal saline control group, DEHP group and vitamin E alone group. The sensitized group of OVA control group was divided into OVA sensitization group, DEHP induced OVA sensitization group, OVA sensitized group treated with DEHP and vitamin E, and OVA sensitized group treated with vitamin E alone. There were 7 experimental groups. The whole experiment period was 18 days, in which the time of exposure to DEHP and vitamin E was 14 days, the sensitization group was sensitized with OVA on the 1st and 11th day (saline injection), and the time of atomization was 4 days. DEHP was administered by stomach in the morning, and vitamin E was repaired in the afternoon. The food was fed twice a day after gavage. In this experiment, the concentration of DEHP was 30mg/kg d, and the concentration of vitamin E repair was 30mg/kg d. The mice in the control group were sensitized with the mixture of 83.33 渭 gOVA and 292mgAl (OH) 3 by intraperitoneal injection and subcutaneous injection, including 200 渭 L intraperitoneal injection and 300 渭 L subcutaneous multi-point injection (5 points each time). The atomization excitation was continuous atomization of saline solution containing 1%OVA for 30 min. Physiological and biochemical indexes such as ROS, GSH, IL-4, IgE were measured after modeling. The results showed that oxidative stress was associated with allergic asthma in mice. The degree of allergic asthma in mice increased when oxidative stress was aggravated, but decreased in mice treated with antioxidants. It is suggested that oxidative stress is an effective way for DEHP to induce allergic asthma in mice.
【学位授予单位】：华中师范大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R114;R562.25

【参考文献】