锰中毒导致鸡肝脏炎症相关因子mRNA表达增加以及肝脏损伤

发布时间：2018-05-08 01:20

本文选题：锰 + 鸡　；参考：《东北农业大学》2015年硕士论文

【摘要】：锰,作为生物体内必需的一种微量元素,广泛分布在多种不同的生物体器官及组织内。微量元素锰在机体的生长发育等方面都发挥着极其重要的作用。然而,金属锰也属于一种常见的环境污染物。当生物体长时间处于在锰环境中,或者吸入过量锰的时候,不仅能够对机体产生不同程度的损伤,还能够引起机体锰中毒,例如,锰中毒能够对神经、消化、泌尿生殖以及免疫系统等正常生理功能造成一定程度的影响。目前,国内外研究锰的毒性相关的实验,多数都是以人和鼠作为研究对象展开的研究,而对于禽类锰毒性的研究和报道却很少。所以,本试验以海蓝鸡为试验动物,我们的试验将180只1日龄健康的海蓝鸡随机分成对照组、低剂量组、中剂量组和高剂量组共四组。对照组中饲喂正常日粮,而将低剂量组、中剂量组、高剂量组分别按锰对鸡半数致死量的染毒量换算成饲料摄取量,进行拌料染锰,使低剂量组、中剂量组、高剂量组中饲喂的日粮锰含量分别达到:600 mg/kg、900 mg/kg和1800mg/kg。在试验进行的第30天、60天、90天每组随机抽取15只鸡,处死后取肝脏组织样。试验内容为观察肝脏组织在光学显微镜和透射电子显微镜下的病理学变化,并检测肝脏组织NO含量和i NOS活性,以及运用实时定量PCR技术对鸡肝脏组织中NF-κB、TNF-α、i NOS、COX-2和PGE2 m RNA表达量进行检测。研究锰过量对鸡肝脏功能产生的影响,并初步探讨锰中毒可能造成的毒理学机制。得出以下结果:(1)根据显微观察和超显微观察的结果,结果显示鸡肝脏组织发生损伤;(2)根据试剂盒测定结果发现,鸡肝脏组织中NO含量增加,i NOS活性升高;(3)实时定量PCR检测的结果显示出,鸡肝脏组织中NF-κB、TNF-α、i NOS、COX-2和PGE2mRNA表达升高。我们的研究结果表明,过量的锰暴露能引起炎症反应,使NF-κB、TNF-α、i NOS、COX-2和PGE2 m RNA表达增加,并且使鸡肝脏组织中NO含量和i NOS活性提高。所得到的结果表明,鸡肝脏中NF-κB途径在锰诱导的炎症反应中起重要作用
[Abstract]:Manganese, as a necessary trace element in organisms, is widely distributed in many different organism organs and tissues. Trace element manganese plays an extremely important role in the growth and development of the body. However, manganese metal is also a common environmental pollutant. When an organism is in a manganese environment for a long time, or when it inhales excessive manganese, it can not only cause varying degrees of damage to the body, but also lead to manganese poisoning in the organism. For example, manganese poisoning can cause nerve, digestion, Normal physiological functions such as genitourinary and immune system are affected to a certain extent. At present, most of the experiments related to manganese toxicity at home and abroad are carried out with human and mouse as the research objects, but there are few studies and reports on poultry manganese toxicity. Therefore, 180 1-day-old healthy sea blue chickens were randomly divided into four groups: control group, low dose group, middle dose group and high dose group. The control group was fed normal diet, and the low dose group, middle dose group and high dose group were converted into feed intake according to the lethal dose of manganese to chicken, respectively, and mixed with manganese to dye manganese, so that the low dose group, the middle dose group, In the high dose group, the manganese content in the diet reached 900 mg/kg and 1800 mg / kg 路kg ~ (-1), respectively, at 1: 600 mg 路kg ~ (-1) 路kg ~ (-1) 路kg ~ (-1). 15 chickens were randomly selected from each group on the 30th day, 60 days and 90 days after the trial. The pathological changes of liver tissue under optical microscope and transmission electron microscope were observed, and the content of no and the activity of I NOS in liver tissue were detected. The expression of COX-2 and PGE2 m RNA in chicken liver tissue was detected by real-time quantitative PCR. To study the effect of manganese excess on liver function of chicken, and to explore the possible toxicological mechanism of manganese poisoning. According to the results of microscopic observation and ultramicroscopic observation, the result shows that the liver tissue of chicken is damaged. The results of real-time quantitative PCR detection showed that the expression of COX-2 and PGE2mRNA in chicken liver tissue was increased. Our results showed that excessive exposure to manganese could induce inflammatory reaction, increase the expression of COX-2 and PGE2 m RNA in NF- 魏 B, TNF- 伪 -TNF- 伪 I, and increase the content of no and the activity of I NOS in chicken liver. The results show that NF- 魏 B pathway plays an important role in manganese induced inflammation in chicken liver.
【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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