| 杜 敏,王 慧,徐萌萌,杨婷婷,李 悦.AQP1在阿霉素肾病大鼠器官水肿中作用研究[J].,2024,(8):1433-1438 |
| AQP1在阿霉素肾病大鼠器官水肿中作用研究 |
| Study on The Role of AQP1 in Organ Edema in Rats with Adriamycin Nephropathy |
| 投稿时间：2023-11-07 修订日期：2023-11-29 |
| DOI：10.13241/j.cnki.pmb.2024.08.005 |
| 中文关键词: 阿霉素肾病 水通道蛋白1 水肿 器官 |
| 英文关键词: Adriamycin nephropathy AQP1 Edema Organ |
| 基金项目:国家自然科学基金项目（82060795）；贵阳中医学院博士启动基金项目（2017） |
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| 中文摘要: |
| 摘要 目的：探究阿霉素肾病是否引起除肾脏外的器官水肿，以及水通道蛋白1（Aquaporin 1，AQP1）的表达变化在器官水肿形成中的作用。方法：将20只SD大鼠随机分为模型组和对照组。模型组予尾静脉注射盐酸阿霉素（6.0 mg/kg）造模，对照组注射等量生理盐水。造模6周后处死，记录体重和心、肝、脾、肺重量，应用HE染色法对心、肝、脾、肺组织进行病理学观察，使用IHC法检测AQP1在心、肝、脾、肺组织的分布，使用Western blot法和RT-PCR法检测各器官组织中AQP1的蛋白和mRNA表达水平。结果：与对照组相比，阿霉素肾病大鼠尿蛋白显著升高（P<0.01），体重显著降低（P<0.05），肺系数显著升高（P<0.05），但心、肝、脾重量没有显著变化。心、肝、肺均出现不同程度的水肿和病理损伤，脾表现出血液充盈不足；免疫组化结果显示AQP1分布于肝脏胆管细胞、心脏肌细胞膜及微血管内皮细胞、脾血红细胞、肺毛细血管内皮细胞。Western blot和RT-PCR结果显示模型组心脏AQP1蛋白和mRNA表达水平均显著增高（P<0.05），肝脏AQP1蛋白表达水平有所升高，但无统计学差异。结论：阿霉素肾病可导致心、肝、肺表现出水肿和不同程度的损伤，还可上调心脏AQP1的表达进而促进心肌水肿的形成。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate whether adriamycin nephropathy causes edema in organs other than kidney and the role of AQP1 expression change in organ edema. Methods: Twenty SD rats were randomly divided into control group and model group. The model group was injected with adriamycin (6.0 mg/kg) via tail vein, and the control group was injected with the same amount of normal saline. The rats were sacrificed after 6 weeks, and the body weight and the weights of heart, liver, spleen, and lung were recorded. The pathology of the heart, liver, spleen, and lung were observed by HE staining. The distribution of AQP1 in heart, liver, spleen, and lung was detected by IHC method. And the protein and mRNA expression of AQP1 in each organ were detected by Western blot and RT-PCR. Results: Compared to the control group, the urinary protein of adriamycin nephropathy rats increased significantly (P<0.01), the body weight decreased significantly (P<0.05), and the lung coefficient increased significantly (P<0.05). Whereas, there were no significant differences in heart, liver, and spleen weights between control and model group. The heart, liver and lung showed different degrees of edema and pathological damage, and the spleen showed insufficient blood filling. The immunohistochemistry results showed that AQP1 was distributed in hepatic cholangiocytes, cardiac myocyte membranes, and microvascular endothelial cells, spleen erythrocyte, and pulmonary capillary endothelial cells. The results of Western blot and RT-PCR showed that the expression of AQP1 protein and mRNA in the heart of the model group was significantly increased (P<0.05). And the expression of AQP1 protein in the liver was increased, but there was no statistically significant difference. Conclusion: Adriamycin nephropathy can cause heart, liver, and lung edema appear different degrees of damage, and up-regulate the expression of AQP1 in the heart to promote the formation of myocardial edema. |
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