| 康 婷,毛海霞,林佳如,朱婷婷,张丽玲,张冬梅,吴蔚桦,欧三桃.自噬在慢性肾病血管钙化中的作用研究[J].中国比较医学杂志,2023,33(1):51~60. |
| 自噬在慢性肾病血管钙化中的作用研究 |
| Effects of autophagy on vascular calcification in chronic kidney disease |
| 投稿时间：2022-06-16 |
| DOI：10. 3969 / j.issn.1671-7856. 2023. 01. 007 |
| 中文关键词: 慢性肾病 血管钙化 动脉平滑肌细胞 自噬 成骨样分化 |
| 英文关键词:chronic kidney disease vascular calcification aorta smooth muscle cell autophagy osteogenic differentiation |
| 基金项目: |
| 作者 | 单位 | | 康 婷 | 1.西南医科大学附属医院肾病内科,四川 泸州 646000
2.四川省肾脏疾病临床医学研究中心,四川 泸州 646000 | | 毛海霞 | 1.西南医科大学附属医院肾病内科,四川 泸州 646000
2.四川省肾脏疾病临床医学研究中心,四川 泸州 646000 | | 林佳如 | 1.西南医科大学附属医院肾病内科,四川 泸州 646000
2.四川省肾脏疾病临床医学研究中心,四川 泸州 646000 | | 朱婷婷 | 1.西南医科大学附属医院肾病内科,四川 泸州 646000
2.四川省肾脏疾病临床医学研究中心,四川 泸州 646000 | | 张丽玲 | 1.西南医科大学附属医院肾病内科,四川 泸州 646000
2.四川省肾脏疾病临床医学研究中心,四川 泸州 646000 | | 张冬梅 | 1.西南医科大学附属医院肾病内科,四川 泸州 646000
2.四川省肾脏疾病临床医学研究中心,四川 泸州 646000 | | 吴蔚桦 | 1.西南医科大学附属医院肾病内科,四川 泸州 646000
2.四川省肾脏疾病临床医学研究中心,四川 泸州 646000 | | 欧三桃 | 1.西南医科大学附属医院肾病内科,四川 泸州 646000
2.四川省肾脏疾病临床医学研究中心,四川 泸州 646000 |
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| Author Name | Affiliation | | KANG Ting | 1.Department of Nephrology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. 2. Sichuan Clinical Research Center for Nephropathy, Luzhou 646000 | | MAO Haixia | 1.Department of Nephrology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. 2. Sichuan Clinical Research Center for Nephropathy, Luzhou 646000 | | LIN Jiaru | 1.Department of Nephrology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. 2. Sichuan Clinical Research Center for Nephropathy, Luzhou 646000 | | ZHU Tingting | 1.Department of Nephrology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. 2. Sichuan Clinical Research Center for Nephropathy, Luzhou 646000 | | ZHANG Liling | 1.Department of Nephrology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. 2. Sichuan Clinical Research Center for Nephropathy, Luzhou 646000 | | ZHANG Dongmei | 1.Department of Nephrology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. 2. Sichuan Clinical Research Center for Nephropathy, Luzhou 646000 | | WU Weihua | 1.Department of Nephrology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. 2. Sichuan Clinical Research Center for Nephropathy, Luzhou 646000 | | OU Santao | 1.Department of Nephrology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. 2. Sichuan Clinical Research Center for Nephropathy, Luzhou 646000 |
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| 中文摘要: |
| 目的 探索自噬与 CKD 血管钙化之间的关系,以及自噬在 CKD 血管钙化中的作用。 方法 首先将 30 只 SD 大鼠随机分为对照组(Control 组,15 只)和腺嘌呤及高磷饮食诱导的模型组(CKD 组,15 只)。 免疫组化检测主动脉中 α-SMA、RUNX2、LC3B 及 Beclin-1 蛋白表达,新鲜主动脉做钙含量测定,进一步做它们之间的相关性分析。再构建 β-GP 诱导的主动脉平滑肌细胞(aorta smooth muscle cell,ASMC)钙化模型。电镜检测细胞内自噬小体,免疫荧光及 Western blot 检测 LC3B 蛋白。自噬抑制剂 3-MA 及激活剂 RAP 干预自噬后,采用免疫组化、 Western blot 检测 ASMC 中 α-SMA、RUNX2 蛋白表达变化,茜素红染色及钙含量检测 ASMC 钙化情况。 结果 模型组成功建立 CKD 血管钙化模型。与对照组相比,模型组主动脉 α-SMA 蛋白表达下降,RUNX2、LC3B、Beclin-1 蛋白表达及钙含量升高。 Beclin-1 及 LC3B 蛋白表达分别与主动脉钙含量及 RUNX2 蛋白表达呈正相关。 β-GP 诱导 ASMC 自噬小体增加,LC3B 荧光斑点增多,LC3BII 蛋白表达增强(P<0. 01)。 RAP 激活自噬后减少 ASMC 钙沉积 及钙含量(P<0. 05),减少 RUNX2 蛋白表达(P<0. 05),促进 α-SMA 蛋白表达(P<0. 05);3-MA 抑制自噬后结果与之相反。 结论 CKD 血管钙化同时存在自噬激活,自噬在 CKD 血管钙化中可能具有内源性保护作用,自噬有望成为 CKD 血管钙化新的治疗靶目标。 |
| 英文摘要: |
| Objective To explore the association and role of autophagy in vascular calcification of chronic kidney disease. Methods Overall, 30 SD rats were randomly divided into a control group (Control group, n= 15) and adenine and high phosphorus diet-induced model group (CKD group, n= 15). Immunohistochemistry was applied to detect α-SMA, RUNX2, LC3B and Beclin-1 in the aorta. Calcium content was measured to further analyze the correlation between them. Aorta smooth muscle cell (ASMC) calcification was induced by β-GP. Autophagy activation was detected by electron microscopy, immunofluorescence, and Western blot. After 3-MA and RAP regulation of autophagy, immunohistochemistry and Western blot were used to detect α-SMA and RUNX2 protein expression, and alizarin red staining and calcium contents were used to detect calcification of ASMC. Results Compared with the control group, vascular calcification was established in the CKD group. RUNX2, LC3B and Beclin-1 proteins, and calcium content were higher in the CKD group than in the control group, while α-SMA protein expression had declined. Correlation analysis showed that Beclin-1 and LC3B protein expression were positively correlated with aortic calcium content and RUNX2 protein expression, respectively. β-GP induced ASMC calcium deposition and osteogenic differentiation. β-GP induced an increase of autophagosomes, LC3B fluorescent spots, and LC3BII protein expression (P<0. 01). After autophagy activation by RAP, calcium deposition and content (P<0. 05) and RUNX2 protein expression (P< 0. 05) were reduced, while α-SMA protein expression was promoted (P<0. 05). After-autophagy inhibition by 3-MA, calcium deposition and content were increased (P< 0. 05), RUNX2 protein expression was promoted ( P< 0. 05 ), and α-SMA protein expression was decreased ( P< 0. 05 ). Conclusions Autophagy might play a protective role in CKD vascular calcification. Autophagy is expected to become a new therapeutic target for CKD vascular calcification. |
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