• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

烟酰胺通过抑制肾小管损伤和炎症来减少肾间质纤维化。

Nicotinamide reduces renal interstitial fibrosis by suppressing tubular injury and inflammation.

机构信息

Department of Nephrology, The Key Laboratory of Kidney Disease and Blood Purification of Hunan Province, Second Xiangya Hospital at Central South University, Changsha, China.

The State Key Laboratory of Medical Genetics, School of Life Sciences, Central South University, Changsha, China.

出版信息

J Cell Mol Med. 2019 Jun;23(6):3995-4004. doi: 10.1111/jcmm.14285. Epub 2019 Apr 16.

DOI:10.1111/jcmm.14285
PMID:30993884
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6533567/
Abstract

Renal interstitial fibrosis is a common pathological feature in progressive kidney diseases currently lacking effective treatment. Nicotinamide (NAM), a member of water-soluble vitamin B family, was recently suggested to have a therapeutic potential for acute kidney injury (AKI) in mice and humans. The effect of NAM on chronic kidney pathologies, including renal fibrosis, is unknown. Here we have tested the effects of NAM on renal interstitial fibrosis using in vivo and in vitro models. In vivo, unilateral urethral obstruction (UUO) induced renal interstitial fibrosis as indicated Masson trichrome staining and expression of pro-fibrotic proteins, which was inhibited by NAM. In UUO, NAM suppressed tubular atrophy and apoptosis. In addition, NAM suppressed UUO-associated T cell and macrophage infiltration and induction of pro-inflammatory cytokines, such as TNF-α and IL-1β. In cultured mouse proximal tubule cells, NAM blocked TGF-β-induced expression of fibrotic proteins, while it marginally suppressed the morphological changes induced by TGF-β. NAM also suppressed the expression of pro-inflammatory cytokines (eg MCP-1 and IL-1β) during TGF-β treatment of these cells. Collectively, the results demonstrate an anti-fibrotic effect of NAM in kidneys, which may involve the suppression of tubular injury and inflammation.

摘要

肾间质纤维化是目前进展性肾脏疾病的一种常见病理特征，缺乏有效的治疗方法。烟酰胺（NAM）是水溶性维生素 B 族的成员，最近有研究表明其对小鼠和人类的急性肾损伤（AKI）具有治疗潜力。NAM 对慢性肾脏疾病的作用，包括肾纤维化，尚不清楚。本研究使用体内和体外模型检测了 NAM 对肾间质纤维化的影响。在体内，单侧输尿管梗阻（UUO）诱导的肾间质纤维化如 Masson 三色染色和促纤维化蛋白的表达，被 NAM 所抑制。在 UUO 中，NAM 抑制了肾小管萎缩和凋亡。此外，NAM 抑制了 UUO 相关的 T 细胞和巨噬细胞浸润以及促炎细胞因子（如 TNF-α和 IL-1β）的诱导。在培养的小鼠近端肾小管细胞中，NAM 阻断了 TGF-β诱导的纤维化蛋白表达，而对 TGF-β诱导的形态变化抑制作用较小。NAM 还抑制了 TGF-β处理这些细胞过程中促炎细胞因子（如 MCP-1 和 IL-1β）的表达。总之，这些结果表明 NAM 对肾脏具有抗纤维化作用，这可能涉及抑制肾小管损伤和炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/d3d0251af9f2/JCMM-23-3995-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/5bb34f7e4e63/JCMM-23-3995-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/51c911136133/JCMM-23-3995-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/80e2f3f66281/JCMM-23-3995-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/571d5167b892/JCMM-23-3995-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/b45c170b28a4/JCMM-23-3995-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/7ff74ff08ffd/JCMM-23-3995-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/d3d0251af9f2/JCMM-23-3995-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/5bb34f7e4e63/JCMM-23-3995-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/51c911136133/JCMM-23-3995-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/80e2f3f66281/JCMM-23-3995-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/571d5167b892/JCMM-23-3995-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/b45c170b28a4/JCMM-23-3995-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/7ff74ff08ffd/JCMM-23-3995-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d4b/6533567/d3d0251af9f2/JCMM-23-3995-g007.jpg

相似文献

1
Nicotinamide reduces renal interstitial fibrosis by suppressing tubular injury and inflammation.烟酰胺通过抑制肾小管损伤和炎症来减少肾间质纤维化。
J Cell Mol Med. 2019 Jun;23(6):3995-4004. doi: 10.1111/jcmm.14285. Epub 2019 Apr 16.
2
Apamin inhibits renal fibrosis via suppressing TGF-β1 and STAT3 signaling in vivo and in vitro.阿帕米胺通过体内和体外抑制 TGF-β1 和 STAT3 信号通路抑制肾纤维化。
J Mol Med (Berl). 2021 Sep;99(9):1265-1277. doi: 10.1007/s00109-021-02087-x. Epub 2021 May 24.
3
Arctigenin suppresses renal interstitial fibrosis in a rat model of obstructive nephropathy.原花青素抑制梗阻性肾病大鼠模型肾间质纤维化。
Phytomedicine. 2017 Jul 1;30:28-41. doi: 10.1016/j.phymed.2017.03.003. Epub 2017 Mar 10.
4
Specific Inhibitor of Smad3 (SIS3) Attenuates Fibrosis, Apoptosis, and Inflammation in Unilateral Ureteral Obstruction Kidneys by Inhibition of Transforming Growth Factor β (TGF-β)/Smad3 Signaling.特异性 Smad3 抑制剂（SIS3）通过抑制转化生长因子 β（TGF-β）/Smad3 信号通路减轻单侧输尿管梗阻肾脏的纤维化、细胞凋亡和炎症。
Med Sci Monit. 2018 Mar 20;24:1633-1641. doi: 10.12659/msm.909236.
5
Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction.单侧输尿管梗阻期间，肾小管细胞中自噬的持续激活会促进肾间质纤维化。
Autophagy. 2016 Jun 2;12(6):976-98. doi: 10.1080/15548627.2016.1166317. Epub 2016 Apr 28.
6
Elsholtzia ciliata (Thunb.) Hylander attenuates renal inflammation and interstitial fibrosis via regulation of TGF-ß and Smad3 expression on unilateral ureteral obstruction rat model.香薷通过调节单侧输尿管梗阻大鼠模型中的TGF-β和Smad3表达减轻肾脏炎症和间质纤维化。
Phytomedicine. 2016 Apr 15;23(4):331-9. doi: 10.1016/j.phymed.2016.01.013. Epub 2016 Feb 11.
7
Hirudin improves renal interstitial fibrosis by reducing renal tubule injury and inflammation in unilateral ureteral obstruction (UUO) mice.水蛭素通过减少单侧输尿管梗阻 (UUO) 小鼠的肾小管损伤和炎症来改善肾间质纤维化。
Int Immunopharmacol. 2020 Apr;81:106249. doi: 10.1016/j.intimp.2020.106249. Epub 2020 Feb 14.
8
Isoliquiritigenin Attenuates UUO-Induced Renal Inflammation and Fibrosis by Inhibiting Mincle/Syk/NF-Kappa B Signaling Pathway.异甘草素通过抑制 Mincle/Syk/NF-κB 信号通路减轻 UUO 诱导的肾脏炎症和纤维化。
Drug Des Devel Ther. 2020 Apr 14;14:1455-1468. doi: 10.2147/DDDT.S243420. eCollection 2020.
9
Increasing cGMP-dependent protein kinase activity attenuates unilateral ureteral obstruction-induced renal fibrosis.增加 cGMP 依赖性蛋白激酶活性可减轻单侧输尿管梗阻诱导的肾纤维化。
Am J Physiol Renal Physiol. 2014 May 1;306(9):F996-1007. doi: 10.1152/ajprenal.00657.2013. Epub 2014 Feb 26.
10
Ruxolitinib Alleviates Renal Interstitial Fibrosis in UUO Mice.罗沙司他减轻 UUO 小鼠的肾间质纤维化。
Int J Biol Sci. 2020 Jan 1;16(2):194-203. doi: 10.7150/ijbs.39024. eCollection 2020.

引用本文的文献

1
Genetic Factors Related to the Development or Progression of Mesoamerican Endemic Nephropathy.与中美洲地方性肾病发生或进展相关的遗传因素
Int J Mol Sci. 2025 May 8;26(10):4486. doi: 10.3390/ijms26104486.
2
NAD+ prevents chronic kidney disease by activating renal tubular metabolism.烟酰胺腺嘌呤二核苷酸（NAD+）通过激活肾小管代谢来预防慢性肾病。
JCI Insight. 2025 Mar 10;10(5):e181443. doi: 10.1172/jci.insight.181443.
3
α-methyltryptophan-mediated protection against diabetic nephropathy in mice as studied with a metabolomics approach.

本文引用的文献

1
Dicer deficiency in proximal tubules exacerbates renal injury and tubulointerstitial fibrosis and upregulates Smad2/3.近端小管中的 Dicer 缺乏会加重肾损伤和肾小管间质纤维化，并上调 Smad2/3。
Am J Physiol Renal Physiol. 2018 Dec 1;315(6):F1822-F1832. doi: 10.1152/ajprenal.00402.2018. Epub 2018 Oct 3.
2
De novo NAD biosynthetic impairment in acute kidney injury in humans.人类急性肾损伤中的从头合成 NAD 生物合成损伤。
Nat Med. 2018 Sep;24(9):1351-1359. doi: 10.1038/s41591-018-0138-z. Epub 2018 Aug 20.
3
Legumain, an asparaginyl endopeptidase, mediates the effect of M2 macrophages on attenuating renal interstitial fibrosis in obstructive nephropathy.
用代谢组学方法研究α-甲基色氨酸对小鼠糖尿病肾病的保护作用。
Front Pharmacol. 2025 Jan 20;15:1463673. doi: 10.3389/fphar.2024.1463673. eCollection 2024.
4
The role and therapeutic targeting of the CCL2/CCR2 signaling axis in inflammatory and fibrotic diseases.CCL2/CCR2信号轴在炎症性和纤维化疾病中的作用及治疗靶点
Front Immunol. 2025 Jan 9;15:1497026. doi: 10.3389/fimmu.2024.1497026. eCollection 2024.
5
NAD metabolism in acute kidney injury and chronic kidney disease transition.急性肾损伤与慢性肾病转变过程中的NAD代谢
Trends Mol Med. 2025 Jul;31(7):669-681. doi: 10.1016/j.molmed.2024.12.004. Epub 2025 Jan 4.
6
NAD enhancers as therapeutic agents in the cardiorenal axis.NAD 增强剂作为心脏肾轴的治疗剂。
Cell Commun Signal. 2024 Nov 8;22(1):537. doi: 10.1186/s12964-024-01903-4.
7
CircPWWP2A promotes renal interstitial fibrosis through modulating miR-182/ROCK1 axis.环状 RNA PWWP2A 通过调控 miR-182/ROCK1 轴促进肾间质纤维化。
Ren Fail. 2024 Dec;46(2):2396455. doi: 10.1080/0886022X.2024.2396455. Epub 2024 Sep 4.
8
Derangement in Nicotinamide Adenine Dinucleotide Metabolism is Observed During Acute Kidney Injury Among Male Agricultural Workers at Risk for Mesoamerican Nephropathy.在有中美洲肾病风险的男性农业工人急性肾损伤期间，观察到烟酰胺腺嘌呤二核苷酸代谢紊乱。
Kidney Int Rep. 2024 Apr 18;9(7):2250-2259. doi: 10.1016/j.ekir.2024.04.027. eCollection 2024 Jul.
9
Therapeutic application of nicotinamide: As a potential target for inhibiting fibrotic scar formation following spinal cord injury.烟酰胺的治疗应用：作为抑制脊髓损伤后纤维疤痕形成的潜在靶点。
CNS Neurosci Ther. 2024 Jul;30(7):e14826. doi: 10.1111/cns.14826.
10
Nicotinamide mitigates visceral leishmaniasis by regulating inflammatory response and enhancing lipid metabolism.烟酰胺通过调节炎症反应和增强脂质代谢来缓解内脏利什曼病。
Parasit Vectors. 2024 Jul 6;17(1):288. doi: 10.1186/s13071-024-06370-x.
组织蛋白酶 S，一种天冬酰胺内肽酶，介导 M2 巨噬细胞减轻梗阻性肾病肾间质纤维化的作用。
Kidney Int. 2018 Jul;94(1):91-101. doi: 10.1016/j.kint.2017.12.025. Epub 2018 Apr 12.
4
Histone deacetylase inhibitors protect against cisplatin-induced acute kidney injury by activating autophagy in proximal tubular cells.组蛋白去乙酰化酶抑制剂通过激活近端肾小管细胞自噬来预防顺铂诱导的急性肾损伤。
Cell Death Dis. 2018 Feb 23;9(3):322. doi: 10.1038/s41419-018-0374-7.
5
Macrophage Uptake of Necrotic Cell DNA Activates the AIM2 Inflammasome to Regulate a Proinflammatory Phenotype in CKD.巨噬细胞摄取坏死细胞 DNA 激活 AIM2 炎性小体调节 CKD 中的促炎表型。
J Am Soc Nephrol. 2018 Apr;29(4):1165-1181. doi: 10.1681/ASN.2017080863. Epub 2018 Feb 9.
6
FGF21 is induced in cisplatin nephrotoxicity to protect against kidney tubular cell injury.成纤维细胞生长因子 21 在顺铂肾毒性中被诱导以防止肾小管细胞损伤。
FASEB J. 2018 Jun;32(6):3423-3433. doi: 10.1096/fj.201701316R. Epub 2018 Jan 22.
7
Proteomic Profiling Reveals the Transglutaminase-2 Externalization Pathway in Kidneys after Unilateral Ureteric Obstruction.蛋白质组学分析揭示了单侧输尿管梗阻后肾脏中转谷氨酰胺酶-2 的外化途径。
J Am Soc Nephrol. 2018 Mar;29(3):880-905. doi: 10.1681/ASN.2017050479. Epub 2018 Jan 30.
8
Renal tubule injury: a driving force toward chronic kidney disease.肾小管损伤：慢性肾脏病的驱动力。
Kidney Int. 2018 Mar;93(3):568-579. doi: 10.1016/j.kint.2017.09.033. Epub 2018 Jan 17.
9
PINK1-PRKN/PARK2 pathway of mitophagy is activated to protect against renal ischemia-reperfusion injury.PINK1-PRKN/PARK2 介导的线粒体自噬途径被激活以保护肾脏免受缺血再灌注损伤。
Autophagy. 2018;14(5):880-897. doi: 10.1080/15548627.2017.1405880. Epub 2018 Feb 17.
10
Mechanisms of Renal Fibrosis.肾脏纤维化的机制。
Annu Rev Physiol. 2018 Feb 10;80:309-326. doi: 10.1146/annurev-physiol-022516-034227. Epub 2017 Oct 25.