DEHP致小鼠哮喘和氧化應(yīng)激關(guān)系的初步研究
發(fā)布時(shí)間：2018-11-18 16:13
【摘要】：DEHP是一種人工合成的化學(xué)物質(zhì),常作為增塑劑添加到塑料制品中,用以增加塑料制品的柔韌性。DEHP的物理性質(zhì)為無(wú)色也基本無(wú)味,不易蒸發(fā)。隨著工業(yè)的發(fā)展,鄰苯二甲酸酯類物質(zhì)比上個(gè)世紀(jì)更密切的貼近我們的生活之中,無(wú)論是居住環(huán)境還是食品、飲用品,乃至醫(yī)療用品中我們都接觸著形形色色的鄰苯二甲酸酯類物質(zhì)。而氧化應(yīng)激反應(yīng)是一個(gè)在機(jī)體普遍發(fā)生的應(yīng)激反應(yīng),它形成的原因多種多樣,它表現(xiàn)的形式千變?nèi)f化,近幾年逐漸成為了熱門話題。在之前的研究中我們已經(jīng)知道DEHP在小鼠的過(guò)敏性哮喘中起到的是佐劑作用。而DEHP也能引起氧化應(yīng)激反應(yīng)的發(fā)生,氧化應(yīng)激是否也是DEHP導(dǎo)致小鼠過(guò)敏性哮喘的途徑現(xiàn)在還沒(méi)有明確的定論。 本論文的研究中,實(shí)驗(yàn)分為兩個(gè)大組,即生理鹽水對(duì)照的非致敏組和OVA對(duì)照的致敏組。其中,生理鹽水對(duì)照的非致敏組又分為生理鹽水對(duì)照組,DEHP染毒組和維生素E單獨(dú)作用組；OVA對(duì)照的致敏組分為OVA單獨(dú)致敏組,DEHP染毒OVA致敏組,DEHP和維生素E聯(lián)合作用OVA致敏組,維生素E單獨(dú)作用OVA致敏組,共7個(gè)實(shí)驗(yàn)組。整個(gè)實(shí)驗(yàn)周期共18天,其中DEHP染毒和維生素E作用的時(shí)間為14天,致敏組在第1天和第11天用OVA致敏(非致敏組注射生理鹽水),霧化激發(fā)期為4天。上午進(jìn)行DEHP灌胃染毒,下午進(jìn)行維生素E灌胃修復(fù)。全天兩次灌胃后進(jìn)行喂食。本實(shí)驗(yàn)中DEHP染毒濃度為30mg/kg·d,維生素E修復(fù)濃度亦為30mg/kg·d,對(duì)照組用生理鹽水灌胃。OVA致敏采用83.33μgOVA和292mgAl(OH)3的混合液500μL對(duì)小鼠腹腔注射和皮下注射混合致敏,其中200μL腹腔注射,300μL皮下多點(diǎn)注射(每次5點(diǎn))。霧化激發(fā)則為含1%OVA的生理鹽水溶液連續(xù)霧化30min。建模后測(cè)量ROS, GSH, IL-4, IgE等生理生化指標(biāo)。 實(shí)驗(yàn)結(jié)果說(shuō)明：氧化應(yīng)激反應(yīng)與小鼠過(guò)敏性哮喘的發(fā)生有相關(guān)性。氧化應(yīng)激反應(yīng)加重時(shí)小鼠過(guò)敏性哮喘程度增加,加入抗氧化劑保護(hù)后的小鼠的過(guò)敏性哮喘程度下降。說(shuō)明氧化應(yīng)激是DEHP導(dǎo)致小鼠過(guò)敏性哮喘的有效途徑。
[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.
【學(xué)位授予單位】：華中師范大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2013
【分類號(hào)】：R114;R562.25
本文編號(hào)：2340509
[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.
【學(xué)位授予單位】：華中師范大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2013
【分類號(hào)】：R114;R562.25
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