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两种由苯并(a)芘和脂多糖诱导的炎症相关肺癌发生的小鼠模型的比较。

The comparison of two mouse models of inflammation-related lung tumorigenesis induced by benzo(a)pyrene and lipopolysaccharide.

机构信息

Department of Toxicology, College of Public Health, Zhengzhou University, No. 100 Kexue Avenue, Zhengzhou, Henan 450001, China.

Department of Bone and soft tissue cancer, The Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), No. 127 Dongming Road, Zhengzhou, Henan 450008, China.

出版信息

Exp Anim. 2019 Aug 14;68(3):301-306. doi: 10.1538/expanim.18-0159. Epub 2019 Mar 12.

Abstract

Inflammation-related animal model is necessary to better understanding the association of inflammation with tumorigenesis. Although mouse models of inflammation-related lung tumorigenesis on A/J mice strain have been set up in previous study, there is no report on the model on C57BL/6J mice. In this study, C57BL/6J mice were randomly divided into two groups and instilled with benzo(a)pyrene [B(a)p] plus lipopolysaccharide (LPS) with different treatments. Mice in Group I were instilled intratracheally with B(a)p (1 mg/mouse) and LPS (5 µg/mouse), once a week for 4 times, on Tuesday and Friday, respectively [the week of the last time of B(a)p treatment named Week 0]. At Week 4, mice continued to be treated with LPS, once every four weeks for 5 times. Mice in Group II were exposed to B(a)p (1 mg/mouse, once a week for 4 times) and 3 weeks later instilled intratracheally with LPS (2.5 µg/mouse) once every three weeks for 5 times. At Week 30, the incidence, number, size and histopathology of lung tumor in two models were compared. The tumor incidence (96.97%) and mean tumor count (13.0 ± 12.4) of mice in Group II were significantly increased compared with those in Group I (69.23%, 4.9 ± 5.1), respectively. In addition, smaller tumors (≤1 mm) were more abundant in Group II than Group I. Histopathological examination found the tumors induced by B(a)p plus LPS in Group II were more advanced tumors. In conclusion, a better mouse model of inflammation-related lung tumorigenesis induced by B(a)p plus LPS in C57BL/6J mice was set up successfully.

摘要

在更好地理解炎症与肿瘤发生之间的关系方面,炎症相关动物模型是必要的。尽管先前的研究已经建立了 A/J 小鼠炎症相关肺肿瘤发生的小鼠模型,但尚未有关于 C57BL/6J 小鼠模型的报道。在本研究中,将 C57BL/6J 小鼠随机分为两组,并以不同的处理方式用苯并(a)芘[B(a)P]加脂多糖(LPS)进行气管内滴注。第 I 组小鼠每周二和周五分别气管内滴注 B(a)P(1mg/只)和 LPS(5μg/只),共 4 次[最后一次 B(a)P 处理的周称为第 0 周]。第 4 周时,小鼠继续用 LPS 处理,每 4 周 1 次,共 5 次。第 II 组小鼠每周接受 B(a)P(1mg/只,共 4 次)处理 3 周后,每周三气管内滴注 LPS(2.5μg/只),共 5 次。第 30 周时,比较了两种模型中肺肿瘤的发生率、数量、大小和组织病理学变化。与第 I 组相比,第 II 组小鼠的肿瘤发生率(96.97%)和平均肿瘤数(13.0±12.4)显著增加。此外,第 II 组中较小的肿瘤(≤1mm)比第 I 组更为丰富。组织病理学检查发现,第 II 组由 B(a)P 加 LPS 诱导的肿瘤为更晚期的肿瘤。总之,成功建立了一种更好的 C57BL/6J 小鼠 B(a)P 加 LPS 诱导的炎症相关肺肿瘤发生模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b958/6699972/07bcdfcbb417/expanim-68-301-g001.jpg

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