本文選題：鋁 + 大鼠��； 參考：《東北農(nóng)業(yè)大學(xué)》2017年碩士論文

【摘要】：本試驗(yàn)以80只5周齡體重約為115 g的Wistar大鼠為實(shí)驗(yàn)動(dòng)物,隨機(jī)均分為4組,分別為對(duì)照組(CG,0 mg/kg B.W.Al Cl3),低劑量組(LG,64 mg/kg B.W.Al Cl3),中劑量組(MG,128 mg/kg B.W.Al Cl3)和高劑量組(HG,256 mg/kg B.W.Al Cl3)。通過(guò)向飲水中添加六水三氯化鋁(Al Cl3·6H2O)方式,復(fù)制鋁中毒模型,實(shí)驗(yàn)期120 d。采用ELISA法檢測(cè)大鼠血清促腎上腺皮質(zhì)激素釋放激素(CRH)、促腎上腺皮質(zhì)激素(ACTH)和糖皮質(zhì)激素(GCs)含量和大鼠脾臟淋巴細(xì)胞內(nèi)caspase-9、caspase-3的活性;流氏細(xì)胞術(shù)檢測(cè)脾臟淋巴細(xì)胞凋亡率;q RT-PCR法檢測(cè)大鼠脾臟淋巴細(xì)胞細(xì)胞中糖皮質(zhì)激素受體(GCR)、NF-κB、Bcl-2、Bax、caspase-9和caspase-3 m RNA表達(dá)量;western blot法檢測(cè)GCR和NF-κB大鼠脾臟淋巴細(xì)胞核蛋白的表達(dá)量。目的在于探討NF-κB在鋁通過(guò)下丘腦-垂體-腎上腺(HPA)軸誘導(dǎo)大鼠脾臟淋巴細(xì)胞凋亡中的作用及機(jī)制,結(jié)果發(fā)現(xiàn):(1)染鋁組大鼠血清CRH、ACTH和GCs的含量均顯著高于對(duì)照組(p0.05,p0.01);脾臟淋巴細(xì)胞內(nèi)GCR m RNA和蛋白表達(dá)量均顯著高于對(duì)照組(p0.05,p0.01),說(shuō)明鋁激活下丘腦-垂體-腎上腺(HPA)軸。(2)染鋁組大鼠脾臟淋巴細(xì)胞早期和晚期凋亡率均顯著高于對(duì)照組(p0.01);Bcl-2/Bax mRNA表達(dá)比率均顯著低于對(duì)照組(p0.05,p0.01);caspase-9和caspase-3 m RNA表達(dá)量和活性均顯著高于對(duì)照組(p0.05,p0.01),說(shuō)明鋁可誘導(dǎo)大鼠脾臟淋巴細(xì)胞凋亡。(3)染鋁組大鼠脾臟淋巴細(xì)胞中NF-κB mRNA和核蛋白表達(dá)量均顯著低于對(duì)照組(p0.01);淋巴細(xì)胞內(nèi)GCR的核蛋白表達(dá)量與NF-κB的核蛋白表達(dá)量呈負(fù)相關(guān);NF-κB mRNA表達(dá)量與Bcl-2 mRNA表達(dá)量呈正相關(guān),而與Bax mRNA表達(dá)量呈負(fù)相關(guān),說(shuō)明NF-κB是鋁通過(guò)HPA軸誘導(dǎo)大鼠脾臟淋巴細(xì)胞凋亡的關(guān)鍵因子。上述結(jié)果說(shuō)明,鋁通過(guò)HPA軸激活NF-κB調(diào)控的大鼠脾臟淋巴細(xì)胞凋亡。研究結(jié)果可為緩解鋁免疫毒性的研究奠定基礎(chǔ)。
[Abstract]:Eighty 5-week-old Wistar rats weighing about 115g were randomly divided into 4 groups: control group (CG 0 mg/kg B.W.Al Cl 3), low dose group (GG + 64 mg/kg B.W.Al Cl 3), middle dose group (MGN 128 mg/kg B.W.Al Cl 3) and high dose group (HGG 256 mg/kg B.W.Al Cl 3). The experimental animals were divided into three groups: the control group, the low dose group and the middle dose group, respectively. The model of aluminum poisoning was established by adding aluminum chloride (Al Cl3 6H 2O) into drinking water for 120 days. The contents of serum corticotropin releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and glucocorticoid (GCs) and the activity of caspase-9 and caspase-3 in rat spleen lymphocytes were measured by ELISA method. Apoptosis rate of splenic lymphocytes was detected by flow cytometry and Q RT-PCR method was used to detect the expression of caspase-9 and caspase-3 m RNA in rat splenic lymphocytes. Western blot method was used to detect the expression of nuclear protein in spleen lymphocytes of GCR and NF- 魏 B rats. Objective to investigate the role and mechanism of NF- 魏 B in apoptosis of spleen lymphocytes in rats induced by aluminum via hypothalamus-pituitary-adrenal (HPA) axis. The results showed that the levels of serum CRHH-ACTH and GCs in the control group were significantly higher than those in the control group, and the expression of GCR m RNA and protein in spleen lymphocytes were significantly higher than those in the control group, indicating that aluminum activated hypothalamus-pituitary-adrenal (HPA) axis. The early and late apoptosis rate of spleen lymphocytes in aluminum exposed group was significantly higher than that in control group, which was significantly lower than that in control group. The expression and activity of caspase-9 and caspase-3 m RNA in control group were significantly higher than those in control group, which indicated that aluminum could induce spleen of rats. The expression of NF- 魏 B mRNA and nuclear protein in spleen lymphocytes of rats exposed to aluminum was significantly lower than that of control group (p0.01), and the expression of GCR in lymphocytes was negatively correlated with the expression of nuclear protein of NF- 魏 B. The expression of Bcl-2 mRNA was positively correlated. The expression of NF- 魏 B was negatively correlated with the expression of Bax mRNA, indicating that NF- 魏 B was the key factor of apoptosis of spleen lymphocytes induced by aluminum through the HPA axis in rats. These results suggest that aluminum activates NF- 魏 B induced apoptosis of spleen lymphocytes through HPA axis. The results may lay a foundation for the study of alleviating the immune toxicity of aluminum.
【學(xué)位授予單位】：東北農(nóng)業(yè)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類(lèi)號(hào)】：R114

【參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 袁嫦靜;王守偉;黃大f ;劉秀梅;王興國(guó);孫寶國(guó);任發(fā)政;;理性、科學(xué)地直面中國(guó)食品安全持久戰(zhàn)(上)——2014年食品安全熱點(diǎn)科學(xué)解讀[J];食品工業(yè)科技;2015年03期

2 張春玲;曹杰;陶俊杰;;2009-2011年鎮(zhèn)江市部分食品中添加劑監(jiān)測(cè)分析[J];江蘇預(yù)防醫(yī)學(xué);2012年06期

3 楊洋;蔡雪婷;曹鵬;;腫瘤的化學(xué)預(yù)防治療靶點(diǎn)——NF-κB[J];中南醫(yī)學(xué)科學(xué)雜志;2012年05期

4 楊文軍;張桂香;;白山市部分市售食品中鋁污染檢測(cè)結(jié)果分析[J];中國(guó)衛(wèi)生工程學(xué);2012年04期

5 龐潔;;鋁對(duì)人體的毒性及相關(guān)食品安全問(wèn)題研究進(jìn)展[J];內(nèi)科;2011年05期

6 李娜;王曉燕;劉春長(zhǎng);張勤麗;牛僑;;caspase-3基因在染鋁小鼠神經(jīng)細(xì)胞凋亡中的作用[J];環(huán)境與職業(yè)醫(yī)學(xué);2011年03期

7 Sara De Iudicibus;Raffaella Franca;Stefano Martelossi;Alessandro Ventura;Giuliana Decorti;;Molecular mechanism of glucocorticoid resistance in inflammatory bowel disease[J];World Journal of Gastroenterology;2011年09期

8 趙瑞杰;李引乾;王會(huì);王廣彬;娜日蘇;金大鵬;關(guān)偉軍;馬月輝;;Caspase家族與細(xì)胞凋亡的關(guān)系[J];中國(guó)畜牧雜志;2010年17期

9 李風(fēng)森;哈木拉提;楊劍;劉慧芳;;糖皮質(zhì)激素對(duì)哮喘患者淋巴細(xì)胞亞群及其介質(zhì)、內(nèi)源性皮質(zhì)醇的影響[J];臨床肺科雜志;2010年06期

10 王德杰;劉興國(guó);張東;;糖皮質(zhì)激素受體的研究進(jìn)展[J];現(xiàn)代生物醫(yī)學(xué)進(jìn)展;2010年08期

相關(guān)博士學(xué)位論文 前3條

1 李婷;PSAP誘導(dǎo)獨(dú)特的不依賴(lài)于Bcl-2家族蛋白的線粒體凋亡途徑[D];吉林大學(xué);2012年

2 胡崇偉;去甲腎上腺素與鋁免疫毒性的關(guān)系[D];東北農(nóng)業(yè)大學(xué);2011年

3 魏翠柏;健腦安對(duì)腦缺血再灌注后高糖皮質(zhì)激素促海馬神經(jīng)細(xì)胞凋亡作用的影響[D];北京中醫(yī)藥大學(xué);2004年

相關(guān)碩士學(xué)位論文 前9條

1 孫旭東;三氯化鋁抑制大鼠骨形成及Wnt/β-catenin信號(hào)轉(zhuǎn)導(dǎo)機(jī)制[D];東北農(nóng)業(yè)大學(xué);2016年

2 王靜;鋁致大鼠淋巴細(xì)胞凋亡的cAMP/PKA信號(hào)傳導(dǎo)機(jī)制[D];東北農(nóng)業(yè)大學(xué);2014年

3 錢(qián)康琦;葛根素對(duì)小鼠成骨細(xì)胞TGF-β/Smad基因蛋白表達(dá)影響的研究[D];南京中醫(yī)藥大學(xué);2014年

4 韓彥飛;三氯化鋁對(duì)體外培養(yǎng)大鼠成骨細(xì)胞的毒性作用[D];東北農(nóng)業(yè)大學(xué);2013年

5 白崇生;CRH、ACTH和GC對(duì)體外培養(yǎng)染鋁大鼠脾淋巴細(xì)胞免疫功能的影響[D];東北農(nóng)業(yè)大學(xué);2013年

6 夏士亮;鋁致大鼠淋巴細(xì)胞凋亡的線粒體/Caspase依賴(lài)性途徑機(jī)制[D];東北農(nóng)業(yè)大學(xué);2013年

7 佘s，

本文編號(hào)：1917085