本文關鍵詞： 硒 雞 主動脈 硒蛋白 抗氧化 炎癥因子 熱休克蛋白　出處：《東北農業(yè)大學》2015年碩士論文　論文類型：學位論文

【摘要】：硒是機體不可缺少的微量元素,廣泛參與體內各種生理生化活動,發(fā)揮著不可替代的作用,硒缺乏可以導致多種疾病的發(fā)生,如心血管疾病,癌癥,肝臟疾病等。硒通過參與構成多種抗氧化酶的活性中心,在體內的抗氧化過程中發(fā)揮著重要作用。硒在生物體內以硒蛋白的形式執(zhí)行其生物學功能,硒可以調節(jié)體內硒蛋白的表達水平和活性;硒缺乏與引起心血管疾病的炎癥有關,硒能夠增強免疫活性細胞的功能,因此被認為是一種抗炎劑。目前,硒的生物學功能受到廣泛重視,硒缺乏對多種臟器的影響已有相關報道,但缺硒對血管損傷的研究報道甚少。血管的病變直接或間接的導致心血管疾病的發(fā)生發(fā)展。本試驗將研究探討缺硒對雛雞主動脈損傷的影響,為硒元素的研究提供重要理論依據。將180只一日齡雛雞隨機分為兩組正常組和缺硒組。缺硒組飼喂含硒量為0.033mg/kg的日糧;正常組飼喂硒含量為0.2 mg/kg的飼料。分別于15d、25d、35d、45d、55d及65d剖殺采集主動脈組織。通過測定抗氧化功能、硒蛋白、炎癥因子以及熱休克蛋白的表達探討缺硒對血管損傷的影響,結果表明:(1)與正常組雛雞相比,缺硒組雛雞伴有典型的硒缺乏臨床癥狀,并且超微結構改變。表明雛雞硒缺乏模型復制成功,并且硒缺乏可導致雛雞主動脈損傷。(2)雛雞硒缺乏會造成主動脈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。表明氧化應激參與了缺硒性動脈損傷的病理過程。(3)硒缺乏可以顯著下調雛雞主動脈中25種硒蛋白mRNA的表達水平,除Gpx4外,它只有在第45d時表達水平顯著下降。(4)缺硒能夠上調雛雞主動脈中炎癥因子的表達,NF-κB、TNF-α、COX-2、PTGEs和i NOS mRNA的表達均顯著增加,NF-κB、COX-2和i NOS的蛋白表達水平也都顯著增加,表明炎癥因子參與了缺硒性動脈損傷的過程。(5)缺硒能夠上調雛雞主動脈中熱休克蛋白的表達水平,Hsp27、Hsp40、Hsp60、Hsp70和Hsp90的mRNA表達水平均顯著增加,Hsp60、Hsp70和Hsp90的蛋白表達水平也都顯著增加。結果表明,熱休克蛋白參與了缺硒性動脈損傷的過程。
[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- 偽 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.
【學位授予單位】：東北農業(yè)大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：S858.31

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相關期刊論文 前1條

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本文編號：1536983