[1]邵 华,张 怡,黄 丽,等.NF1和p-ERK1/2蛋白在苯并芘联合脂多糖诱导的小鼠肺癌中的表达[J].郑州大学学报(医学版),2019,(06):835-839.[doi:10.13705/j.issn.1671-6825.2018.12.048]
 SHAO Hua,ZHANG Yi,HUANG Li,et al.Expressions of NF1 and p-ERK1/2 in B(a)p and LPS-induced lung cancer in mice[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2019,(06):835-839.[doi:10.13705/j.issn.1671-6825.2018.12.048]
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NF1和p-ERK1/2蛋白在苯并芘联合脂多糖诱导的小鼠肺癌中的表达()
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《郑州大学学报(医学版)》[ISSN:1671-6825/CN:41-1340/R]

卷:
期数:
2019年06期
页码:
835-839
栏目:
论著
出版日期:
2019-11-20

文章信息/Info

Title:
Expressions of NF1 and p-ERK1/2 in B(a)p and LPS-induced lung cancer in mice
作者:
邵 华张 怡黄 丽高 敏冯斐斐
郑州大学公共卫生学院卫生毒理学教研室 郑州 450001
Author(s):
SHAO HuaZHANG YiHUANG LiGAO MinFENG Feifei
Department of Toxicology, College of Public Health, Zhengzhou University, Zhengzhou 450001
关键词:
神经纤维瘤蛋白1 细胞外信号调节激酶1/2 肺癌 小鼠
Keywords:
neurofibromatosis 1 ERK1/2 lung cancer mouse
分类号:
R114
DOI:
10.13705/j.issn.1671-6825.2018.12.048
摘要:
目的:探讨神经纤维瘤蛋白1(NF1)和磷酸化细胞外信号调节激酶1/2(p-ERK1/2)在苯并芘[(B(a)P)]联合脂多糖(LPS)诱导的小鼠肺癌中的表达。方法:SPF级C57BL/6 小鼠随机分为4组:对照组、B(a)p组、LPS组和B(a)p+LPS组。B(a)p+LPS组小鼠经气管滴注50 μL溶于三辛酸甘油酯中的B(a)p(1 mg/只),每周1次,连续4周后停止,此时计为第0周; 于第3周经气管滴注50 μL溶于生理盐水中的LPS(2.5 μg/只),每3周1次,连续给予5次。B(a)p组和LPS组小鼠分别按相应的方式进行染毒,对照组小鼠经肺灌注等体积的三辛酸甘油酯和生理盐水。正常饲养至30周解剖观察小鼠肺癌发生情况,免疫组化法检测小鼠肺组织中NF1和p-ERK1/2蛋白的表达。结果:对照组和LPS组小鼠肺部未见肿瘤; 与B(a)p组相比,B(a)p+LPS组小鼠的肿瘤形成率升高,平均肿瘤形成数增加(P<0.05)。与对照组相比,B(a)p+LPS组、B(a)p组肺癌组织中NF1蛋白表达降低,p-ERK1/2蛋白表达升高(P<0.05); NF1与p-ERK1/2蛋白在B(a)P+LPS组相关系数为-0.771(P=0.015)。结论:LPS能够促进B(a)p诱导的小鼠肺癌发生,且NF1和p-ERK1/2参与了炎性相关肺癌的发生。
Abstract:
Aim:To investigate the expressions of neurofibromatosis 1(NF1)and phosphorylated extracellular signal regulated kinase 1/2(p-ERK1/2)in B(a)p and LPS-induced lung cancer in mice.Methods:The specific pathogen free C57BL/6 mice were randomly allocated into control group,B(a)p group,LPS group and B(a)p plus LPS group.The mice in B(a)p plus LPS group were instilled intratracheally with B(a)p(1 mg/mouse,dissolved in 50 μL tricaptin)once a week for four times [the week of the last time of B(a)p treatment named Week 0].At week 3,mice were instilled intratracheally with LPS(2.5 μg/mouse,dissolved in 50 μL saline)once every three weeks for 5 times.Moreover the mice in B(a)p and LPS groups were administered B(a)p or LPS respectively in a similar manner,and the mice in control group were given equal volume of the tricaptin and saline.After 30 weeks, the mice were dissected to observe the occurrence of lung cancer. The expressions of NF1 and p-ERK1/2 proteins in lung tissue were detected by immunohistochemical SP method.Results:No tumors were observed in lung tissue of control group and LPS group.Compared with B(a)p group, the tumor incidence and mean tumor count in B(a)p plus LPS group were significantly increased(P<0.05).Compared with control group, the expression of NF1 protein in B(a)p plus LPS group and B(a)p group was decreased, and the expression of p-ERK1/2 protein was increased(P<0.05).Negative correlation between the expression of NF1 protein and that of p-ERK1/2 protein in lung cancer tissue of B(a)P+LPS group was observed,and the pearson correlation coefficient was -0.771(P=0.015).Conclusion:LPS could enhance the occurrence of lung cancer in mice induced by B(a)p,and NF1 and p-ERK1/2 may involve in the pathogenesis of inflammation-related lung cancer.

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备注/Memo

备注/Memo:
【基金项目】国家自然科学青年基金项目(81402712); 郑州大学青年骨干教师培养计划项目(2017ZDGGJS039) 【作者简介】冯斐斐,通信作者,女,1983年4月生,博士,副教授,研究方向:环境毒理分子机制,E-mail:feifeifeng@zzu.edu.cn
更新日期/Last Update: 2019-11-20