BALB/c小鼠蛋白质营养不良:一种类似临床情景的实验模型

IF 0.3 Q3 MEDICINE, GENERAL & INTERNAL Journal of Health and Allied Sciences NU Pub Date : 2022-12-05 DOI:10.1055/s-0042-1758526
V. D’souza, Madhura Rj, Megha Shetty, V. A., Anirban Chakraborthy, M. B, V. A., Murali Badanthadka
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摘要

目的建立一种稳定的类似人类的营养不良实验小鼠模型,为今后的实验研究奠定基础。在断奶时,将雌性BALB/c小鼠分为两组:一组接受低蛋白饲粮(LPD, 10%蛋白质),另一组接受市售的正常颗粒饲粮(ND, 18%蛋白质)。采用体重指数(BMI)、葡萄糖、天冬氨酸转氨酶、丙氨酸转氨酶、碱性磷酸酶、总蛋白、白蛋白、总胆固醇、钙和磷等生化指标(研究第12周和第15周的血清样本)、抗氧化测定和肝脏组织病理学观察来评估模型的发育和稳定性。采用安乐死后切除肝组织进行抗氧化试验及组织病理学观察。结果根据Gomez的营养不良分类原则,根据体重变化对ND的影响,将LPD小鼠划分为营养不良一级。营养不良组BMI的长期显著下降表明稳定的营养不良模型的发展。第15周血清酶水平升高和抗氧化活性降低提示营养不良组在细胞水平出现肝损伤和氧化应激。肝组织的组织病理学改变进一步强化了在营养不良人群中所报道的这些观察结果。结论本研究证实了使用LPD(10%蛋白质)建立稳定的营养不良实验模型的可行性。该模型可用于研究营养不良在任何疾病的病理生理、药物作用及其动力学中的作用。
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Protein Malnutrition in BALB/c Mice: An Experimental Model Resembling Clinical Scenario
Abstract Objectives  The study aims to develop a stable malnourished experimental mice model resembling the human population for future experimental studies. Materials and Methodology  At weaning, female BALB/c mice are separated into two groups: one receiving a low protein diet (LPD, 10% protein) and the other receiving a commercially available normal pellet diet (ND, 18% protein). Model development and stability were assessed using body mass index (BMI), biochemical parameters such as glucose, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total protein, albumin, total cholesterol, calcium, and phosphorus using serum samples at the 12th and 15th weeks of the study, antioxidant assay, and liver histopathology observation. Antioxidant assay and histopathology observation using liver tissue sample excised after euthanasia. Results  LPD mice are categorized under grade I malnutrition based on the body weight change with respect to ND as per the principles of Gomez's classification of malnutrition. A significant long-term decrease in BMI of the malnourished group indicates the development of the stable malnourished model. Elevated serum enzyme levels in the 15th week and decreased antioxidant activity suggest liver injury and oxidative stress at the cellular level in the malnourished group. Histopathology alterations in the liver tissue further strengthen these observations reported in the human population of malnutrition. Conclusion  This study confirms the development of a stable malnourished experimental model using a LPD (10% protein). This model may be used to study the role of malnutrition in the pathophysiology of any disease, drug action, and its kinetics in the future.
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Journal of Health and Allied Sciences NU
Journal of Health and Allied Sciences NU MEDICINE, GENERAL & INTERNAL-
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