FGF-21对D-gal诱导的小鼠肝脏氧化应激及凋亡保护机制研究
将小鼠随机分为4组,第1组为正常组,第2-4组为D-半乳糖（D-gal）模型组。每天用低剂量（1 mg·kg-1）和高剂量（5 mg·kg-1）FGF-21分别对3、4组模型小鼠进行治疗。7周后,检测小鼠肝脏中ROS、MDA含量,确定小鼠氧化应激水平。检测肝脏细胞核内Nrf2含量及其下游抗氧化酶SOD、CAT、GSH-Px、T-AOC活性,利用Real-time PCR检测Nrf2下游抗氧化基因转录量变化。肝脏进行病理学切片,观察不同组小鼠肝脏凋亡细胞数量变化。检测PI3K、Akt含量,并对PI3K/Akt通路调控的下游抗凋亡蛋白Bcl-2以及促凋亡蛋白Bax、Caspase-3表达量进行检测...
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| Published in | 东北农业大学学报 Vol. 46; no. 8; pp. 61 - 69 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | Chinese |
| Published |
东北农业大学生命科学学院,哈尔滨,150030
2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1005-9369 |
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| Abstract | 将小鼠随机分为4组,第1组为正常组,第2-4组为D-半乳糖（D-gal）模型组。每天用低剂量（1 mg·kg-1）和高剂量（5 mg·kg-1）FGF-21分别对3、4组模型小鼠进行治疗。7周后,检测小鼠肝脏中ROS、MDA含量,确定小鼠氧化应激水平。检测肝脏细胞核内Nrf2含量及其下游抗氧化酶SOD、CAT、GSH-Px、T-AOC活性,利用Real-time PCR检测Nrf2下游抗氧化基因转录量变化。肝脏进行病理学切片,观察不同组小鼠肝脏凋亡细胞数量变化。检测PI3K、Akt含量,并对PI3K/Akt通路调控的下游抗凋亡蛋白Bcl-2以及促凋亡蛋白Bax、Caspase-3表达量进行检测。结果表明：与模型组相比,FGF-21治疗组小鼠肝脏ROS、MDA含量均下降;Nrf2含量上升,其下游抗氧化酶活性上升,抗氧化基因转录量增加;PI3K、Akt含量下降,其下游Bcl-2蛋白表达量增加,Bax、Caspase-3表达量下降。从分子水平揭示FGF-21对小鼠肝脏的保护机制,为脂肪肝或其他肝病的治疗提供参考。 |
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| AbstractList | Q816; 将小鼠随机分为4组,第1组为正常组,第2-4组为D-半乳糖(D-gal)模型组.每天用低剂量(1mg·kg-1)和高剂量(5 mg·kg-1)FGF-21分别对3、4组模型小鼠进行治疗.7周后,检测小鼠肝脏中ROS、MDA含量,确定小鼠氧化应激水平.检测肝脏细胞核内Nrf2含量及其下游抗氧化酶SOD、CAT、GSH-Px、T-AOC活性,利用Real-time PCR检测Nrf2下游抗氧化基因转录量变化.肝脏进行病理学切片,观察不同组小鼠肝脏凋亡细胞数量变化.检测PI3K、Akt含量,并对PI3K/Akt通路调控的下游抗凋亡蛋白Bcl-2以及促凋亡蛋白Bax、Caspase-3表达量进行检测.结果表明:与模型组相比,FGF-21治疗组小鼠肝脏ROS、MDA含量均下降;Nrf2含量上升,其下游抗氧化酶活性上升,抗氧化基因转录量增加;PI3K、Akt含量下降,其下游Bcl-2蛋白表达量增加,Bax、Caspase-3表达量下降.从分子水平揭示FGF-21对小鼠肝脏的保护机制,为脂肪肝或其他肝病的治疗提供参考. 将小鼠随机分为4组,第1组为正常组,第2-4组为D-半乳糖（D-gal）模型组。每天用低剂量（1 mg·kg-1）和高剂量（5 mg·kg-1）FGF-21分别对3、4组模型小鼠进行治疗。7周后,检测小鼠肝脏中ROS、MDA含量,确定小鼠氧化应激水平。检测肝脏细胞核内Nrf2含量及其下游抗氧化酶SOD、CAT、GSH-Px、T-AOC活性,利用Real-time PCR检测Nrf2下游抗氧化基因转录量变化。肝脏进行病理学切片,观察不同组小鼠肝脏凋亡细胞数量变化。检测PI3K、Akt含量,并对PI3K/Akt通路调控的下游抗凋亡蛋白Bcl-2以及促凋亡蛋白Bax、Caspase-3表达量进行检测。结果表明：与模型组相比,FGF-21治疗组小鼠肝脏ROS、MDA含量均下降;Nrf2含量上升,其下游抗氧化酶活性上升,抗氧化基因转录量增加;PI3K、Akt含量下降,其下游Bcl-2蛋白表达量增加,Bax、Caspase-3表达量下降。从分子水平揭示FGF-21对小鼠肝脏的保护机制,为脂肪肝或其他肝病的治疗提供参考。 |
| Author | 任桂萍 衣春霖 杨永碧 于引航 尹杰超 李德山 |
| AuthorAffiliation | 东北农业大学生命科学学院,哈尔滨150030 |
| AuthorAffiliation_xml | – name: 东北农业大学生命科学学院,哈尔滨,150030 |
| Author_FL | REN Guiping YU Yinhang LI Deshan YI Chunlin YIN Jiechao YANG Yongbi |
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| Copyright | Copyright © Wanfang Data Co. Ltd. All Rights Reserved. |
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| DocumentTitleAlternate | Study on protection mechanisms of FGF-21 on mouse liver oxidative stress and apoptosis induced by D-gal |
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| EndPage | 69 |
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| Keywords | Nrf2 氧化应激 apoptosis FGF-21 凋亡 Nrf2,PI3K/Akt oxidative stress FGF21 PI3K/Akt |
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| Notes | REN Guiping, YI Chunlin, YANG Yongbi, YU Yinhang, YIN Jiechao, LI Deshan（School of Life Sciences, Northeast Agricultural University, Harbin 150030, China） Mice were randomly divided into four groups. The first group was a normal group, the 2nd to the 4th groups were builded with D-gal. The 3rd and 4th groups mice were respectively treated with low doses （1 mg- kg1） FGF-21 and high dose （5 mg- kg1） FGF-21. After seven weeks, testing the ROS, MDA levels in liver to determine the level of oxidative stress. The Nrf2 in liver cell nucleus and its downstream antioxidant enzymes SOD, CAT, GSH-Px, T-AOC activity also were detected. The downstream antioxidant gene expression of Nrf2 was detected by Real-time PCR. The number of apoptotic cell in different groups of mouse livers was observed by pathological section. The contents of PI3K and Akt were detected, and the PI3K/Akt pathway downstream antiapoptotic protein Bcl-2 and proapoptotic protein Bax, Caspase-3 was used to detect the expression. Results showed that the c |
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| PublicationTitle | 东北农业大学学报 |
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| PublicationYear | 2015 |
| Publisher | 东北农业大学生命科学学院,哈尔滨,150030 |
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| Snippet | 将小鼠随机分为4组,第1组为正常组,第2-4组为D-半乳糖（D-gal）模型组。每天用低剂量（1 mg·kg-1）和高剂量（5 mg·kg-1）FGF-21分别对3、4组模型小鼠进行治疗。7周后,检测小鼠... Q816; 将小鼠随机分为4组,第1组为正常组,第2-4组为D-半乳糖(D-gal)模型组.每天用低剂量(1mg·kg-1)和高剂量(5 mg·kg-1)FGF-21分别对3、4组模型小鼠进行治疗.7周后,检测小鼠... |
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| SubjectTerms | FGF21 Nrf2 PI3K/Akt 凋亡 氧化应激 |
| Title | FGF-21对D-gal诱导的小鼠肝脏氧化应激及凋亡保护机制研究 |
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