Application value of neutrophil gelatinase associated lipocalin in clinical diagnosis of Crohn's disease

doi:10.11958/20240286

Abstract

Abstract:

Crohn's disease (CD) is an autoimmune intestinal disease characterised by chronic and non-specific inflammation, and the exact etiology and pathogenesis are still unclear. Neutrophil gelatinase associated lipocalin (NGAL), a secreted glycoprotein and isolated from neutrophils, is widely involved in pathophysiological processes such as intestinal inflammation response, apoptosis and tumour progression. It has been found that NGAL has the potential to be a clinical biological marker in clinical diagnosis and monitoring of CD activity. Therefore, this paper reviews the application value of NGAL in different clinical samples of CD, in order to provide reference for clinical diagnosis and treatment of CD.

Key words: Crohn disease, lipocalin-2, diagnosis, neutrophil gelatinase associated lipocalin

CLC Number:

R574

Figures/Tables 1

References 41

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作者	研究类型	参与机制	研究结论
Gupta等^[19]	基础研究	NF-κB/STAT1及细胞自噬	上调NGAL的表达可降低RPE细胞自噬，抑制NGAL表达可减少AMD的发生
Yao等^[20]	基础研究	LIFR/NK-κB/LCN2及铁死亡	抑制NK-κB调控的NGAL表达，调控铁死亡进展，改善肝癌病程
Kim等^[21]	基础研究	α-SMA/MMP9/STAT3	NGAL通过α-SMA/MMP9/STAT3信号通路，促进NASH进展
Wang等^[22]	基础研究	MAPK/ERK及铁死亡	抑制NGAL可干扰MAPK/ERK信号通路，减轻ARDS炎症反应和氧化应激损伤
Huang等^[23]	基础研究	铁死亡	NGAL诱导铁死亡，加重心功能障碍进展
Luo等^[24]	基础研究	NF-κB/STAT3及铁死亡	NGAL通过NF-κB/STAT3信号通路促进脑损伤神经元铁死亡
Yadav等^[25]	基础研究	NF-κB信号通路	促炎因子通过NF-κB诱导NGAL表达，NGAL是MS肠炎及菌群失调的标志物
Zollner等^[26]	病例对照研究	-	NGAL在CD中高表达，与FC、CRP、ESR呈显著正相关
Thorsvik等^[27]	病例对照研究	-	NGAL在CD中高表达，与FC、CRP、ESR呈显著正相关
Hsieh等^[28]	基础研究	-	粪便NGAL是小鼠CD模型的标志物
Komaru等^[29]	前瞻性研究	-	尿液NGAL是预测重症急性肾损伤的生物标志物
Manfredi等^[30]	前瞻性研究	-	MMP-9/NGAL是CD临床诊断的潜在标志物
Bolignano等^[31]	横断面研究	TNF-α介导Th1反应	IFX抑制TNF-α的表达，下调Th1介导的NGAL的产生
Janas等^[32]	病例对照研究	-	NGAL诱发肠道氧化应激反应，加重肠上皮损伤，且其水平与CD活动性呈正相关
Korkmaz等^[33]	病例对照研究	-	NGAL诱发肠道氧化应激反应，加重肠上皮损伤，且其水平与CD活动性呈正相关
Stallhofer等^[34]	病例对照研究	IL-23/Th17轴	炎性因子通过IL-23/Th17轴促进肠上皮细胞产生NGAL

作者	研究类型	参与机制	研究结论
Gupta等^[19]	基础研究	NF-κB/STAT1及细胞自噬	上调NGAL的表达可降低RPE细胞自噬，抑制NGAL表达可减少AMD的发生
Yao等^[20]	基础研究	LIFR/NK-κB/LCN2及铁死亡	抑制NK-κB调控的NGAL表达，调控铁死亡进展，改善肝癌病程
Kim等^[21]	基础研究	α-SMA/MMP9/STAT3	NGAL通过α-SMA/MMP9/STAT3信号通路，促进NASH进展
Wang等^[22]	基础研究	MAPK/ERK及铁死亡	抑制NGAL可干扰MAPK/ERK信号通路，减轻ARDS炎症反应和氧化应激损伤
Huang等^[23]	基础研究	铁死亡	NGAL诱导铁死亡，加重心功能障碍进展
Luo等^[24]	基础研究	NF-κB/STAT3及铁死亡	NGAL通过NF-κB/STAT3信号通路促进脑损伤神经元铁死亡
Yadav等^[25]	基础研究	NF-κB信号通路	促炎因子通过NF-κB诱导NGAL表达，NGAL是MS肠炎及菌群失调的标志物
Zollner等^[26]	病例对照研究	-	NGAL在CD中高表达，与FC、CRP、ESR呈显著正相关
Thorsvik等^[27]	病例对照研究	-	NGAL在CD中高表达，与FC、CRP、ESR呈显著正相关
Hsieh等^[28]	基础研究	-	粪便NGAL是小鼠CD模型的标志物
Komaru等^[29]	前瞻性研究	-	尿液NGAL是预测重症急性肾损伤的生物标志物
Manfredi等^[30]	前瞻性研究	-	MMP-9/NGAL是CD临床诊断的潜在标志物
Bolignano等^[31]	横断面研究	TNF-α介导Th1反应	IFX抑制TNF-α的表达，下调Th1介导的NGAL的产生
Janas等^[32]	病例对照研究	-	NGAL诱发肠道氧化应激反应，加重肠上皮损伤，且其水平与CD活动性呈正相关
Korkmaz等^[33]	病例对照研究	-	NGAL诱发肠道氧化应激反应，加重肠上皮损伤，且其水平与CD活动性呈正相关
Stallhofer等^[34]	病例对照研究	IL-23/Th17轴	炎性因子通过IL-23/Th17轴促进肠上皮细胞产生NGAL