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通过一种可控且持续释放乙醇的装置模拟慢性酒精效应。

Mimicking chronic alcohol effects through a controlled and sustained ethanol release device.

作者信息

Kim Wanil, Chu Jin-Ok, Kim Do-Yeon, Lee Soo-Hyeon, Choi Chang-Hyung, Lee Kyung-Ha

机构信息

Department of Biochemistry and Institute of Medical Science, School of Medicine, Gyeongsang National University, Jinju, 52727, Republic of Korea.

Department of Cosmetic Science and Technology, Daegu Haany University, Gyeongsan, 38610, Republic of Korea.

出版信息

J Biol Eng. 2024 May 7;18(1):31. doi: 10.1186/s13036-024-00428-1.

DOI:10.1186/s13036-024-00428-1
PMID:38715085
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11077717/
Abstract

Alcohol consumption, a pervasive societal issue, poses considerable health risks and socioeconomic consequences. Alcohol-induced hepatic disorders, such as fatty liver disease, alcoholic hepatitis, chronic hepatitis, liver fibrosis, and cirrhosis, underscore the need for comprehensive research. Existing challenges in mimicking chronic alcohol exposure in cellular systems, attributed to ethanol evaporation, necessitate innovative approaches. In this study, we developed a simple, reusable, and controllable device for examining the physiological reactions of hepatocytes to long-term alcohol exposure. Our approach involved a novel device designed to continuously release ethanol into the culture medium, maintaining a consistent ethanol concentration over several days. We evaluated device performance by examining gene expression patterns and cytokine secretion alterations during long-term exposure to ethanol. These patterns were correlated with those observed in patients with alcoholic hepatitis. Our results suggest that our ethanol-releasing device can be used as a valuable tool to study the mechanisms of chronic alcohol-mediated hepatic diseases at the cellular level. Our device offers a practical solution for studying chronic alcohol exposure, providing a reliable platform for cellular research. This innovative tool holds promise for advancing our understanding of the molecular processes involved in chronic alcohol-mediated hepatic diseases. Future research avenues should explore broader applications and potential implications for predicting and treating alcohol-related illnesses.

摘要

饮酒是一个普遍存在的社会问题,会带来相当大的健康风险和社会经济后果。酒精引起的肝脏疾病,如脂肪肝、酒精性肝炎、慢性肝炎、肝纤维化和肝硬化,凸显了进行全面研究的必要性。由于乙醇蒸发,在细胞系统中模拟慢性酒精暴露存在现有挑战,因此需要创新方法。在本研究中,我们开发了一种简单、可重复使用且可控的装置,用于检测肝细胞对长期酒精暴露的生理反应。我们的方法涉及一种新型装置,该装置设计用于将乙醇持续释放到培养基中,在数天内保持一致的乙醇浓度。我们通过检测长期暴露于乙醇期间的基因表达模式和细胞因子分泌变化来评估装置性能。这些模式与酒精性肝炎患者中观察到的模式相关。我们的结果表明,我们的乙醇释放装置可作为一种有价值的工具,用于在细胞水平研究慢性酒精介导的肝脏疾病的机制。我们的装置为研究慢性酒精暴露提供了一个实用的解决方案,为细胞研究提供了一个可靠的平台。这种创新工具有望增进我们对慢性酒精介导的肝脏疾病所涉及分子过程的理解。未来的研究途径应探索更广泛的应用以及对预测和治疗酒精相关疾病的潜在影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/de3dc59509d5/13036_2024_428_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/687ebf855a9e/13036_2024_428_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/a5267573170b/13036_2024_428_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/273f04d956a8/13036_2024_428_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/ebf40648e13c/13036_2024_428_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/de3dc59509d5/13036_2024_428_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/687ebf855a9e/13036_2024_428_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/a5267573170b/13036_2024_428_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/273f04d956a8/13036_2024_428_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/ebf40648e13c/13036_2024_428_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8b5/11077717/de3dc59509d5/13036_2024_428_Fig5_HTML.jpg

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本文引用的文献

1
The Global Burden of Liver Disease.《全球肝脏疾病负担》
Clin Gastroenterol Hepatol. 2023 Jul;21(8):1978-1991. doi: 10.1016/j.cgh.2023.04.015. Epub 2023 Apr 28.
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Alcohol-Associated Hepatitis.酒精性肝炎
N Engl J Med. 2022 Dec 29;387(26):2436-2448. doi: 10.1056/NEJMra2207599.
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Alcohol-induced Death Rates in the United States, 2019-2020.2019-2020 年美国因酒精导致的死亡率。
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G-CSF promotes the viability and angiogenesis of injured liver via direct effects on the liver cells.G-CSF 通过直接作用于肝细胞促进受损肝脏的存活和血管生成。
Mol Biol Rep. 2022 Sep;49(9):8715-8725. doi: 10.1007/s11033-022-07715-4. Epub 2022 Jul 4.
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Hepatocyte-derived VEGFA accelerates the progression of non-alcoholic fatty liver disease to hepatocellular carcinoma via activating hepatic stellate cells.肝细胞衍生的 VEGFA 通过激活肝星状细胞加速非酒精性脂肪性肝病向肝细胞癌的进展。
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Antiangiogenic Drugs in NASH: Evidence of a Possible New Therapeutic Approach.非酒精性脂肪性肝炎中的抗血管生成药物:一种可能的新治疗方法的证据
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Oncostatin M promotes hepatic progenitor cell activation and hepatocarcinogenesis via macrophage-derived tumor necrosis factor-α.抑瘤素 M 通过巨噬细胞来源的肿瘤坏死因子-α促进肝祖细胞激活和肝癌发生。
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Chronic Alcohol Exposure of Cells Using Controlled Alcohol-Releasing Capillaries.采用控释毛细管使细胞持续暴露于酒精中。
Cells. 2021 May 6;10(5):1120. doi: 10.3390/cells10051120.
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Role of ALDH2 in Hepatic Disorders: Gene Polymorphism and Disease Pathogenesis.乙醛脱氢酶2在肝脏疾病中的作用:基因多态性与疾病发病机制
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Unraveling the Role of Leptin in Liver Function and Its Relationship with Liver Diseases.解析瘦素在肝功能中的作用及其与肝脏疾病的关系。
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