急性马兜铃酸肾病小鼠C-Myc和Cyclin D1的表达变化
Changes in the Expression of C-Myc and Cyclin D1 in Mice with Acute Aristolochic Acid Nephropathy
DOI: 10.12677/acm.2024.1441220, PDF,   
作者: 兰爱琳, 王一凡, 李小芬, 黄春华, 楼迪栋*:贵州中医药大学基础医学院法医学教研室,贵州 贵阳
关键词: 马兜铃酸I马兜铃酸肾病细胞周期Aristolochic Acid I Aristolochic Acid Nephropathy Cell Cycle
摘要: 为探索急性马兜铃酸肾病(Aristolochic Acid Nephropathy, AAN)过程中细胞损伤后的再生与修复,本实验将40只KM小鼠分为5组:对照组、AAI暴露2、4、6、8天组,AAI组小鼠以5 mg/kg/2d AAI灌胃模拟AAN,使各组小鼠AAI累积剂量分别为5、10、15、20 mg/kg。分别于AAI暴露2、4、6、8天处死,观察肾脏病理学改变,并进行免疫组化染色观察C-myc和Cyclin D1蛋白表达情况。结果显示,与对照组相比,AAI组小鼠C-myc于第2天开始下降,第4天、6天、8天上升;Cyclin D1于AAI暴露第2天、4天下降,第6天、8天升高。本研究可得出结论暴露于AAI的小鼠C-myc和Cyclin D1蛋白表达随AAI累积剂量增加呈“先降后升”趋势。
Abstract: In order to explore the regeneration and repair of cells after cell injury in the course of acute aristolochic acid nephropathy (AAN), 40 KM mice were divided into five groups in this experiment: the control group, the AAI-exposed group for 2, 4, 6, and 8 days, and the mice in the AAI group were simulated by gavage with 5 mg/kg/2d AAI to mimic the acute aristolochic acid nephropathy (AAN), so that the cumulative dose of AAI in each group was 5, 10, 15 and 20 mg/kg, respectively. Mice in the AAI group were put to death on 2, 4, 6 and 8 days of AAI exposure to observe the pathological changes in the kidneys, and immunohistochemistry staining was carried out to observe the protein expression of C-myc and Cyclin D1. The results showed that compared with the control group, C-myc started to decrease on day 2 and increased on days 4, 6, and 8 in the AAI group of mice; Cyclin D1 decreased on days 2 and 4 and increased on days 6 and 8 of AAI exposure. In this study, it can be concluded that the protein expression of C-myc and Cyclin D1 in AAI-exposed mice showed a tendency of “decreasing and then increasing” with the cumulative dose of AAI.
文章引用:兰爱琳, 王一凡, 李小芬, 黄春华, 楼迪栋. 急性马兜铃酸肾病小鼠C-Myc和Cyclin D1的表达变化[J]. 临床医学进展, 2024, 14(4): 1749-1754. https://doi.org/10.12677/acm.2024.1441220

参考文献

[1] Zhou, Q., Jiang, L., Su, T., et al. (2023) Overview of Aristolochic Acid Nephropathy: An Update. Kidney Research and Clinical Practice, 42, 579-590. [Google Scholar] [CrossRef] [PubMed]
[2] 王一凡, 刘爽, 汪思齐, 等. 急性马兜铃酸中毒小鼠肾损伤及Wnt7b/β-catenin/MMP-7的表达变化[J]. 中国医科大学学报, 2023, 52(6): 505-511.
[3] Yu, J., Liu, D., Sun, X., et al. (2019) CDX2 Inhibits the Proliferation and Tumor Formation of Colon Cancer Cells by Suppressing Wnt/β-Catenin Signaling via Transactivation of GSK-3β and Axin2 Expression. Cell Death & Disease, 10, Article No. 26. [Google Scholar] [CrossRef] [PubMed]
[4] Ji, H., Hu, J., Zhang, G., et al. (2021) Aristolochic Acid Nephropathy: A Scientometric Analysis of Literature Published from 1971 to 2019. Medicine, 100, e26510. [Google Scholar] [CrossRef
[5] Toback, F.G. (1992) Regeneration after Acute Tubular Necrosis. Kidney International, 41, 226-246. [Google Scholar] [CrossRef] [PubMed]
[6] Frazier, K.S., Seely, J.C., Hard, G.C., et al. (2012) Proliferative and Nonproliferative Lesions of the Rat and Mouse Urinary System. Toxicologic Pathology, 40, 14s-86s. [Google Scholar] [CrossRef] [PubMed]
[7] Otsuka, M., Hatakenaka, M., Ishigami, K., et al. (2001) Expression of the c-myc and c-fos Genes as a Potential Indicator of Late Radiation Damage to the Kidney. International Journal of Radiation Oncology, Biology, Physics, 49, 169-173. [Google Scholar] [CrossRef
[8] Shen, Y., Miao, N., Wang, B., et al. (2017) c-Myc Promotes Renal Fibrosis by Inducing Integrin αv-Mediated Transforming Growth Factor-β Signaling. Kidney International, 92, 888-899. [Google Scholar] [CrossRef] [PubMed]
[9] Zhang, W., Deng, W. and Wang, Y. (2019) microRNA-103 Promotes LPS-Induced Inflammatory Injury by Targeting c-Myc in HK-2 Cells. Artificial Cells, Nanomedicine, and Biotechnology, 47, 2791-2799. [Google Scholar] [CrossRef] [PubMed]
[10] Osaki, Y., Manolopoulou, M., Ivanova, A.V., et al. (2022) Blocking Cell Cycle Progression through CDK4/6 Protects against Chronic Kidney Disease. JCI Insight, 7. [Google Scholar] [CrossRef] [PubMed]
[11] Kashani, K., Al-Khafaji, A., Ardiles, T., et al. (2013) Discovery and Validation of Cell Cycle Arrest Biomarkers in Human Acute Kidney Injury. Critical Care (London, England), 17, Article No. R25. [Google Scholar] [CrossRef] [PubMed]
[12] Chang-Panesso, M., Kadyrov, F.F., Lalli, M., et al. (2019) FOXM1 Drives Proximal Tubule Proliferation during Repair from Acute Ischemic Kidney Injury. The Journal of Clinical Investigation, 129, 5501-5517. [Google Scholar] [CrossRef