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尿酸肾病中细胞自噬与炎性小体之间的关联。

Association between mitophagy and inflammasome in uric acid nephropathy.

作者信息

Li Xiao-Qian, Gu Yong-Qing, Ling Yuan-Yuan, Wang Mei, Miao Jin, Xue Li, Ji Wei, Liu Jun

机构信息

Department of Nephrology, Nantong Hospital to Nanjing University of Chinese Medicine, Nantong Hospital of Traditional Chinese Medicine, Nantong, Jiangsu, China.

Department of Cardiology, Nantong Hospital to Nanjing University of Chinese Medicine, Nantong Hospital of Traditional Chinese Medicine, Nantong, Jiangsu, China.

出版信息

Ren Fail. 2024 Dec;46(2):2438847. doi: 10.1080/0886022X.2024.2438847. Epub 2024 Dec 16.

DOI:10.1080/0886022X.2024.2438847
PMID:39681479
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11650439/
Abstract

OBJECTIVE

This study was recruited to investigate the role of mitophagy in activating NLRP3 inflammasome in the kidney of uric acid (UA) nephropathy (UAN) rats.

METHODS

This study developed a uric acid nephropathy (UAN) rat model divided into five groups: Negative control (NC), UAN model (M), UAN + autophagy inhibitor (3-MA), UAN + lysosome inhibitor (CQ), and ROS scavenger (N-acetylcysteine, N). H&E staining assessed renal structure, ROS levels were measured with 2, 7dichlorofluorescin diacetate, and ELISA measured serum markers (, , cystatin , , , ). Western blot and qRT-PCR evaluated autophagy and inflammation-related protein (, , , , , , ) expression. NRK-52E cells treated with uric acid and shRNA were analyzed by western blot.

RESULTS

Renal injury in UAN rats was aggravated by ROS accumulation, which promoted mitophagy and activated the inflammasome. Eliminating ROS reduced mitophagy, inhibited NLRP3 activation, lowered and levels, and alleviated renal injury. Notably, inhibiting mitophagy increased ROS accumulation, up-regulated , , and expression, further worsening renal injury. In vitro, uric acid treatment of NRK-52E cells altered autophagy-related protein and pro-inflammatory cytokine levels, highlighting the interplay between mitophagy and inflammation in uric acid nephropathy.

CONCLUSION

Mitophagy influences renal injury in uric acid nephropathy (UAN) by regulating ROS accumulation and inflammasome activation, suggesting that mitophagy may serve as a potential therapeutic target for UAN.

摘要

目的

本研究旨在探讨线粒体自噬在尿酸（UA）肾病（UAN）大鼠肾脏中激活NLRP3炎性小体的作用。

方法

本研究建立了尿酸肾病（UAN）大鼠模型，分为五组：阴性对照（NC）组、UAN模型（M）组、UAN + 自噬抑制剂（3-MA）组、UAN + 溶酶体抑制剂（CQ）组和ROS清除剂（N-乙酰半胱氨酸，N）组。苏木精-伊红（H&E）染色评估肾脏结构，用二乙酸二氯荧光素测定ROS水平，酶联免疫吸附测定（ELISA）检测血清标志物（ ， ，胱抑素 ， ， ）。蛋白质免疫印迹法（Western blot）和实时定量聚合酶链反应（qRT-PCR）评估自噬和炎症相关蛋白（ ， ， ， ， ， ）的表达。用蛋白质免疫印迹法分析用尿酸和短发夹RNA（shRNA）处理的NRK-52E细胞。

结果

UAN大鼠的肾损伤因ROS积累而加重，ROS积累促进了线粒体自噬并激活了炎性小体。清除ROS可减少线粒体自噬，抑制NLRP3激活，降低 和 水平，并减轻肾损伤。值得注意的是，抑制线粒体自噬会增加ROS积累，上调 、 和 的表达，进一步加重肾损伤。在体外，尿酸处理NRK-52E细胞改变了自噬相关蛋白和促炎细胞因子水平，突出了线粒体自噬与尿酸肾病炎症之间的相互作用。

结论

线粒体自噬通过调节ROS积累和炎性小体激活影响尿酸肾病（UAN）的肾损伤，提示线粒体自噬可能是UAN的一个潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/8652b0534f68/IRNF_A_2438847_F0008_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/53136a4b4025/IRNF_A_2438847_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/83e9dafc92b6/IRNF_A_2438847_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/8b8e7be5295c/IRNF_A_2438847_F0003_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/38da9f3b422e/IRNF_A_2438847_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/dab7dd5832df/IRNF_A_2438847_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/265f8bf3d32e/IRNF_A_2438847_F0006_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/34d870d05e5f/IRNF_A_2438847_F0007_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/8652b0534f68/IRNF_A_2438847_F0008_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/53136a4b4025/IRNF_A_2438847_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/83e9dafc92b6/IRNF_A_2438847_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/8b8e7be5295c/IRNF_A_2438847_F0003_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/38da9f3b422e/IRNF_A_2438847_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/dab7dd5832df/IRNF_A_2438847_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/265f8bf3d32e/IRNF_A_2438847_F0006_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/34d870d05e5f/IRNF_A_2438847_F0007_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37a4/11650439/8652b0534f68/IRNF_A_2438847_F0008_C.jpg

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