NLRP3炎性小体在高尿酸血症肾病中作用的研究进展

doi:10.16352/j.issn.1001-6325.2023.02.322

基础医学与临床 ›› 2023, Vol. 43 ›› Issue (2): 322-326.doi: 10.16352/j.issn.1001-6325.2023.02.322

NLRP3炎性小体在高尿酸血症肾病中作用的研究进展

代志新^1*, 王玉敏²

1.赤峰学院附属医院全科医疗科, 内蒙古赤峰 024005;
2.航天中心医院/北京大学航天临床医学院呼吸与危重症医学科, 北京 100049

收稿日期:2021-11-03 修回日期:2022-04-12 出版日期:2023-02-05 发布日期:2023-02-02
通讯作者: ^*1370572086@qq.com
基金资助:
内蒙古自然科学基金(2020MS08175,2021MS08131,2021LHMS08024); 内蒙古自治区高校科研项目(NJZY19218);航天中心医院院级课题(YN202104)

Progress on the role of NLRP3 inflammasome in hyperuricemic nephropathy

DAI Zhixin^1*, WANG Yumin²

1. Department of General Family Medicine, the Affiliated Hospital of Chifeng University, Chifeng 024005;
2. Department of Respiratory and Critical Care Medicine,Aerospace Center Hospital,Peking University Aerospace School of Clinical Medicine, Beijing 100049, China

Received:2021-11-03 Revised:2022-04-12 Online:2023-02-05 Published:2023-02-02
Contact: ^*1370572086@qq.com

摘要/Abstract

摘要： 高尿酸血症肾病(HN)是高尿酸血症(HU)常见的临床并发症,可导致HU相关的肾脏异常。本文阐述与HN相关机制,强调了核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎性小体激活在HN发生和发展中的作用,指出药物靶向抑制NLRP3炎性小体激活是HN的治疗靶点。

关键词: 高尿酸血症肾病, 高尿酸血症, NLRP3炎性小体, 抑制剂

Abstract: Hyperuricemic nephropathy (HN) is a common clinical complication of hyperuricemia, leading to hyperuricemia-associated renal abnormalities. The present review sheds light on the mechanistic aspects pertaining to HN, emphasizing the role of nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome activation in the occurrence and development of HN.This review recommends pharmacological inhibition of NLRP3 infammasome as a therapeutic strategy of HN treatment.

Key words: hyperuricemic nephropathy, hyperuricemia, NLRP3 inflammasome, inhibitor

中图分类号:

R589.7

代志新, 王玉敏. NLRP3炎性小体在高尿酸血症肾病中作用的研究进展[J]. 基础医学与临床, 2023, 43(2): 322-326.

DAI Zhixin, WANG Yumin. Progress on the role of NLRP3 inflammasome in hyperuricemic nephropathy[J]. Basic & Clinical Medicine, 2023, 43(2): 322-326.

参考文献 25

[1]	Komori H, Yamada K, Tamai I. Hyperuricemia enhances intracellular urate accumulation via down-regulation of cell-surface BCRP/ABCG2 expression in vascular endothelial cells[J]. Biochim Biophys Acta Biomembr, 2018,1860:973-980.
[2]	Hong Q, Qi K, Feng Z, et al. Hyperuricemia induces endothelial dysfunction via mitochondrial Na+/Ca2+ exchanger-mediated mitochondrial calcium overload[J]. Cell Calcium, 2012,51:402-10.
[3]	Verzola D, Ratto E, Villaggio B, et al. Uric acid promotes apoptosis in human proximal tubule cells by oxidative stress and the activation of NADPH oxidase NOX 4[J]. PLoS One, 2014,9:e115210.doi: 10.1371/journal.pone.0115210.
[4]	Kang DH. Hyperuricemia and progression of chronic kidney disease: role of phenotype transition of renal tubular and endothelial cells[J]. Contrib Nephrol, 2018,192:48-55.
[5]	Alberts BM, Bruce C, Basnayake K, et al. Secretion of IL-1β from monocytes in gout is redox independent[J]. Front Immunol, 2019,10:70. doi: 10.3389/fimmu.2019.00070.
[6]	Wang M, Zhao J, Zhang N, et al. Astilbin improves potassium oxonate-induced hyperuricemia and kidney injury through regulating oxidative stress and inflammation response in mice[J]. Biomed Pharmacother, 2016,83:975-988.
[7]	Yang Q, Fu C, Xiao J, et al. Uric acid upregulates the adiponectin-adiponectin receptor 1 pathway in renal proximal tubule epithelial cells[J]. Mol Med Rep, 2018,17:3545-3554.
[8]	Yang Q, Fu C, Zhang X, et al. Adiponectin protects against uric acid-induced renal tubular epithelial inflammatory responses via the AdipoR1/AMPK signaling pathway[J]. Int J Mol Med, 2019,43:1542-1552.
[9]	Wang MX, Liu YL, Yang Y, et al. Nuciferine restores potassium oxonate-induced hyperuricemia and kidney inflammation in mice[J]. Eur J Pharmacol, 2015,747:59-70.
[10]	Yang Y, Zhang DM, Liu JH, et al. Wuling San protects kidney dysfunction by inhibiting renal TLR4/MyD88 signaling and NLRP3 inflammasome activation in high fructose-induced hyperuricemic mice[J]. J Ethnopharmacol, 2015,169:49-59.
[11]	Ma CH, Kang LL, Ren HM, et al. Simiao pill ameliorates renal glomerular injury via increasing Sirt1 expression and suppressing NF-κB/NLRP3 inflammasome activation in high fructose-fed rats[J]. J Ethnopharmacol, 2015,172:108-117.
[12]	Wang R, Ma CH, Zhou F, et al. Siwu decoction attenuates oxonate-induced hyperuricemia and kidney inflammation in mice[J]. Chin J Nat Med, 2016,14:499-507.
[13]	Hongyan L, Suling W, Weina Z, et al. Antihyperuricemic effect of liquiritigenin in potassium oxonate-induced hyperuricemic rats[J]. Biomed Pharmacother, 2016,84:1930-1936.
[14]	Chen L, Lan Z. Polydatin attenuates potassium oxonate-induced hyperuricemia and kidney inflammation by inhibiting NF-κB/NLRP3 inflammasome activation via the AMPK/SIRT1 pathway[J]. Food Funct, 2017,8:1785-1792.
[15]	Wu H, Zhou M, Lu G, et al. Emodinol ameliorates urate nephropathy by regulating renal organic ion transporters and inhibiting immune inflammatory responses in rats[J]. Biomed Pharmacother, 2017,96:727-735.
[16]	Hu J, Wu H, Wang D, et al. Weicao capsule ameliorates renal injury through increasing autophagy and NLRP3 degradation in UAN rats[J]. Int J Biochem Cell Biol, 2018,96:1-8.
[17]	Li G, Guan C, Xu L, et al. Scutellarin ameliorates renal injury via increasing CCN1 expression and suppressing NLRP3 inflammasome activation in hyperuricemic mice[J]. Front Pharmacol, 2020,11:584942.doi: 10.3389/fphar.2020.584942.
[18]	Wang YJ, Chen YY, Hsiao CM, et al. Induction of autophagy by pterostilbene contributes to the prevention of renal fibrosis via attenuating NLRP3 inflammasome activation and epithelial-mesenchymal transition[J]. Front Cell Dev Biol, 2020,8:436.doi: 10.3389/fcell.2020.00436.
[19]	Chen Y, Li C, Duan S, et al. Curcumin attenuates potassium oxonate-induced hyperuricemia and kidney inflammation in mice[J]. Biomed Pharmacother, 2019,118:109195. doi: 10.1016/j.biopha.2019.109195.
[20]	Tan J, Wan L, Chen X, et al. Conjugated linoleic acid ameliorates high fructose-induced hyperuricemia and renal inflammation in rats via NLRP3 inflammasome and TLR4 signaling pathway[J]. Mol Nutr Food Res, 2019,63:e1801402. doi: 10.1002/mnfr.201801402.
[21]	Chang YH, Chiang YF, Chen HY, et al. Anti-iinflammatory and anti-hyperuricemic effects of chrysin on a high fructose corn syrup-induced hyperuricemia rat model via the amelioration of urate transporters and inhibition of NLRP3 inflammasome signaling pathway[J]. Antioxidants (Basel), 2021,10.doi: 10.3390/antiox10040564.
[22]	Xu L, Lin G, Yu Q, et al. Anti-hyperuricemic and nephroprotective effects of dihydroberberine in potassium oxonate- and hypoxanthine-induced hyperuricemic mice[J]. Front Pharmacol, 2021,12:645879.doi: 10.3389/fphar.2021.645879.
[23]	Zhou X, Zhang B, Zhao X, et al. Chlorogenic acid supplementation ameliorates hyperuricemia, relieves renal inflammation, and modulates intestinal homeostasis[J]. Food Funct, 2021,12:5637-5649.
[24]	Zhang X, Nie Q, Zhang Z, et al. Resveratrol affects the expression of uric acid transporter by improving inflammation[J]. Mol Med Rep, 2021,2.doi: 10.3892/mmr.2021.12203.
[25]	Sun ZR, Liu HR, Hu D, et al. Ellagic acid exerts beneficial effects on hyperuricemia by inhibiting xanthine oxidase and NLRP3 inflammasome activation[J]. J Agric Food Chem, 2021,9:12741-12752.

NLRP3炎性小体在高尿酸血症肾病中作用的研究进展

Progress on the role of NLRP3 inflammasome in hyperuricemic nephropathy

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献 25

相关文章 15

编辑推荐

Metrics

本文评价

[1]	曲大鹏, 孙会艳, 李强, 王洪权. 铁死亡在蛛网膜下腔出血早期脑损伤发病机制中作用的研究进展[J]. 基础医学与临床, 2023, 43(3): 486-489.
[2]	王斐, 李文轩, 丁俊琼, 刘珍, 王晓明, 杨菊, 王大连. 一氧化氮合酶抑制剂减轻哮喘模型小鼠气道炎性反应[J]. 基础医学与临床, 2023, 43(3): 462-467.
[3]	方思尹, 刘辰, 吴晋晖. 微管抑制剂在血管新生性疾病中的作用机制研究进展[J]. 基础医学与临床, 2023, 43(2): 327-331.
[4]	王平, 徐作军, 徐凯峰. 肺多发结节囊性病变罕见原因结节性硬化症1例[J]. 基础医学与临床, 2022, 42(9): 1424-1427.
[5]	胡宝丽, 胡斌. 罗沙司他治疗肾性贫血的研究进展[J]. 基础医学与临床, 2022, 42(9): 1449-1453.
[6]	甘兹颖, 唐慧. 溶瘤病毒联合PD-1/PD-L1抑制剂的研究进展[J]. 基础医学与临床, 2022, 42(4): 651-655.
[7]	鲍敏, 林玫, 甄海宁, 何芳, 丁敏, 袁竹青, 陈亚隽, 薛欣欣. 醛糖还原酶抑制剂抑制屋尘螨诱导的人支气管上皮细胞系BEAS-2氧化应激反应[J]. 基础医学与临床, 2022, 42(4): 616-621.
[8]	斯晓燕, 王汉萍, 张力, 王孟昭, 张晓彤. 免疫检查点抑制剂致细胞因子释放综合征1例[J]. 基础医学与临床, 2022, 42(11): 1764-1766.
[9]	邵枝定, 高雪, 任婧, 唐晓磊. 5-羟色胺受体适配子的筛选及其抗抑郁功能[J]. 基础医学与临床, 2022, 42(10): 1514-1521.
[10]	陈胜, 王春明, 严雪飞, 毛渊青. 特异性坏死性凋亡抑制剂-1(Nec-1)减轻脊髓损伤模型大鼠胶质瘢痕的形成[J]. 基础医学与临床, 2022, 42(1): 94-99.
[11]	李阳芳, 胡慧敏. PTTG和p21作为无功能垂体瘤放射治疗预后的分子标志物[J]. 基础医学与临床, 2021, 41(9): 1253-1259.
[12]	张若曦, 韩冰. 免疫检查点抑制剂治疗骨髓增生异常综合征的研究进展[J]. 基础医学与临床, 2021, 41(8): 1210-1215.
[13]	郭希, 赖莘秀, 杨媚滟, 李峤桢, 王思行, 宋章永. 抑制侵袭性真菌的新型分子及其作用靶点研究进展[J]. 基础医学与临床, 2021, 41(6): 904-908.
[14]	高峰, 贾梦真, 孙玥. 奥美拉唑治疗对反流性食管炎模型大鼠食管菌群构成的影响[J]. 基础医学与临床, 2021, 41(3): 370-375.
[15]	曹琼, 徐凝馨, 李小文, 吴昊, 郝建卿, 覃艳红, 李莉. 伴CSF1R-Y571D突变的急性髓系白血病细胞系GDM-1的增殖机制[J]. 基础医学与临床, 2021, 41(1): 44-49.