缺硒对雏鸡主动脉炎症因子及热休克蛋白表达的影响

发布时间：2018-02-26 07:08

本文关键词： 硒鸡主动脉硒蛋白抗氧化炎症因子热休克蛋白　出处：《东北农业大学》2015年硕士论文　论文类型：学位论文

【摘要】：硒是机体不可缺少的微量元素,广泛参与体内各种生理生化活动,发挥着不可替代的作用,硒缺乏可以导致多种疾病的发生,如心血管疾病,癌症,肝脏疾病等。硒通过参与构成多种抗氧化酶的活性中心,在体内的抗氧化过程中发挥着重要作用。硒在生物体内以硒蛋白的形式执行其生物学功能,硒可以调节体内硒蛋白的表达水平和活性;硒缺乏与引起心血管疾病的炎症有关,硒能够增强免疫活性细胞的功能,因此被认为是一种抗炎剂。目前,硒的生物学功能受到广泛重视,硒缺乏对多种脏器的影响已有相关报道,但缺硒对血管损伤的研究报道甚少。血管的病变直接或间接的导致心血管疾病的发生发展。本试验将研究探讨缺硒对雏鸡主动脉损伤的影响,为硒元素的研究提供重要理论依据。将180只一日龄雏鸡随机分为两组正常组和缺硒组。缺硒组饲喂含硒量为0.033mg/kg的日粮;正常组饲喂硒含量为0.2 mg/kg的饲料。分别于15d、25d、35d、45d、55d及65d剖杀采集主动脉组织。通过测定抗氧化功能、硒蛋白、炎症因子以及热休克蛋白的表达探讨缺硒对血管损伤的影响,结果表明:(1)与正常组雏鸡相比,缺硒组雏鸡伴有典型的硒缺乏临床症状,并且超微结构改变。表明雏鸡硒缺乏模型复制成功,并且硒缺乏可导致雏鸡主动脉损伤。(2)雏鸡硒缺乏会造成主动脉GSH含量下降,MDA和NO含量升高,Gpx和CAT活性下降,i NOS活性上升。表明氧化应激参与了缺硒性动脉损伤的病理过程。(3)硒缺乏可以显著下调雏鸡主动脉中25种硒蛋白mRNA的表达水平,除Gpx4外,它只有在第45d时表达水平显著下降。(4)缺硒能够上调雏鸡主动脉中炎症因子的表达,NF-κB、TNF-α、COX-2、PTGEs和i NOS mRNA的表达均显著增加,NF-κB、COX-2和i NOS的蛋白表达水平也都显著增加,表明炎症因子参与了缺硒性动脉损伤的过程。(5)缺硒能够上调雏鸡主动脉中热休克蛋白的表达水平,Hsp27、Hsp40、Hsp60、Hsp70和Hsp90的mRNA表达水平均显著增加,Hsp60、Hsp70和Hsp90的蛋白表达水平也都显著增加。结果表明,热休克蛋白参与了缺硒性动脉损伤的过程。
[Abstract]:Selenium is an indispensable trace element in the body, widely participate in various physiological and biochemical activities in the body, play an irreplaceable role, selenium deficiency can lead to a variety of diseases, such as cardiovascular disease, cancer, Liver diseases, etc. Selenium plays an important role in the antioxidant process by participating in the active centers of various antioxidant enzymes. Selenium performs its biological functions in the form of selenium proteins in organisms. Selenium regulates the expression and activity of selenium proteins in the body; selenium deficiency is associated with inflammation that causes cardiovascular disease, and selenium enhances the function of immune active cells, so it is considered to be an anti-inflammatory agent. The biological function of selenium has received extensive attention, and the effects of selenium deficiency on various organs have been reported. However, there are few studies on the effects of selenium deficiency on vascular injury. The pathological changes of blood vessels directly or indirectly lead to the occurrence and development of cardiovascular disease. This study will investigate the effects of selenium deficiency on aortic injury in chicks. 180 one-day-old chicks were randomly divided into two groups: normal group and selenium deficient group. Selenium deficient group was fed with a diet of 0.033 mg / kg selenium. The normal group was fed with a diet containing 0.2 mg/kg of selenium. The aortic tissues were collected at 15 d, 25 d, 35 d, 45 d, 55 d and 65 d, respectively. The effects of selenium deficiency on vascular injury were investigated by measuring the antioxidant function, the expression of selenium protein, inflammatory factor and heat shock protein. The results showed that compared with normal chicks, Se-deficient chicks had typical clinical symptoms of se deficiency and ultrastructural changes, which indicated that the model of se deficiency in chicks was successfully duplicated. Se deficiency can cause aortic injury in chicks. (2) selenium deficiency can cause the decrease of GSH content in aorta and the increase of no content in aorta. The activity of GPX and CAT decreases. It is suggested that oxidative stress is involved in the injury of selenium-deficient arteries. Se deficiency could significantly down-regulate the expression of 25 selenoprotein mRNA in the aorta of chicks. Except for Gpx4, its expression level decreased significantly only at the 45th day.) se deficiency could up-regulate the expression of inflammatory cytokines in the aorta of chicks. Both the expression of PTGEs and I NOS mRNA of TNF- 魏 B, TNF- 伪 OX-2 and I NOS mRNA were significantly increased, and the protein expression of COX-2 and I NOS were also significantly increased. These results indicate that the inflammatory factors are involved in the process of selenium-deficient arterial injury. (5) se deficiency can up-regulate the expression of heat shock protein in the aorta of chicks. Both the mRNA expression levels of Hsp27, Hsp40, Hsp60, Hsp70 and Hsp90 are significantly increased, and the protein expressions of Hsp60, Hsp70 and Hsp90 are also significantly increased. Increase... results show that. Heat shock proteins (HSPs) are involved in se-deficient arterial injury.
【学位授予单位】：东北农业大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：S858.31

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