[1]张燕琴,董菲艳,刘学锋.泛素特异性肽酶20通过调节TGF-β1/SMAD 3级联反应缓解脓毒症性急性肺损伤中的氧化应激和炎症[J].福建医药杂志,2024,46(08):75-78,87.[doi:10.20148/j.fmj.2024.08.022]
点击复制

泛素特异性肽酶20通过调节TGF-β1/SMAD 3级联反应缓解脓毒症性急性肺损伤中的氧化应激和炎症()
分享到:

《福建医药杂志》[ISSN:1002-2600/CN:35-1071/R]

卷:
46
期数:
2024年08期
页码:
75-78,87
栏目:
基础研究
出版日期:
2024-12-20

文章信息/Info

文章编号:
1002-2600(2024)08-0075-04
作者:
张燕琴董菲艳刘学锋
宁德师范学院附属宁德市医院,宁德 352000
关键词:
脓毒性急性肺损伤 USP20 炎症 氧化应激
分类号:
R563.1
DOI:
10.20148/j.fmj.2024.08.022
文献标志码:
A
摘要:
目的 本研究旨在探讨泛素特异性肽酶20(USP20)在脓毒症性急性肺损伤(ALI)中的作用及具体机制。方法 分别用BEAS-2B细胞和C57BL/6小鼠建立体内和体外脂多糖(LPS)处理的ALI模型。RT-qPCR检测USP20的表达情况,在体外实验模型中转染USP20腺病毒后,通过ELISA、CCK8和蛋白质印迹等方法观察其对ALI细胞模型的炎症、氧化应激、生存力等的影响。在USP20过表达治疗后的体内模型中,进一步观察病理变化情况。结果 在ALI小鼠模型、LPS处理的BEAS-2B细胞中证实低表达USP20; 上调USP20可阻止炎症和氧化应激,同时增强了LPS处理的BEAS-2B细胞的生存能力; 上调的USP20通过抑制TGF-β1/SMAD3级联激活减轻ALI小鼠的肺损伤。结论 USP20通过调节TGF-β1/SMAD3级联反应缓解脓毒症性ALI的氧化应激和炎症。

参考文献/References:

[1] 彭海伦,赵月丽,徐崇孝,等.成人脓毒症分型研究进展[J].解放军医学杂志,2023,48(9):1107-1112.
[2] TOMITA K, SAITO Y, SUZUKI T, et al. Vascular endothe-lial growth factor contributes to lung vascular hyperpermeability in sepsis-associated acute lung injury[J].Naunyn Schmiedebergs Arch Pharmacol, 2020, 393(12):2365-2374.
[3] JING R, XIE X, LIAO X, et al. Transforming growth factor-β1 is associated with inflammatory resolution via regulating macrophage polarization in lung injury model mice[J].Int Immunopharmacol, 2024, 142: 112997.
[4] ZHANG J, GUO Y, MAK M, et al. Translational medicine for acute lung injury [J].J Transl Med, 2024, 22(1):25.
[5] 陈文胜,刘文明.脓毒症诱发肝损伤的发病机制研究进展[J].江苏大学学报(医学版),2023,33(2):112-117.
[6] CHEN H Y, HO Y J, CHOU H C, et al. TGF-β1 signaling protects retinal ganglion cells from oxidative stress via modulation of the HO-1/Nrf2 pathway[J].Chem Biol Interact, 2020, 331(0):109249.
[7] KIM J H, SEO D, KIM S J, et al. The deubiquitinating enzyme USP20 stabilizesULK1 and promotes autophagy initiation[J].EMBO Rep,2018,19(4):e44378.
[8] 方玲玉,侯令密,陈艳茹,等.乳腺癌组织中USP20与Ezrin表达的相关性及临床意义[J].现代肿瘤医学,2023,31(15):2850-2854.
[9] ZHANG M X, CAI Z, ZHANG M, et al. USP20 promotes cellular antiviral responsesvia deconjugating K48-Linked Ubiquitination of MITA [J].J Immunol,2019,202(8):2397-2406.
[10] 钟睿梓,张悦,黄晓珺.去泛素化酶USP20与胆固醇结石[J].中国医学创新,2024,21(2):179-183.
[11] 张碧莹,路明,林菲,等.细菌性肝脓肿并发脓毒症的临床特征[J].中国临床药理学杂志,2023,39(3):307-311.
[12] SUN B, LEI M, ZHANG J, et al. Acute lung injury caused by sepsis: how does it happen?[J].Front Med(Lausanne), 2023, 10: 1289194.
[13] MILARA J, PEIR T, SERRANO A, et al. Epithelial to mesenchymal transition is increased in patients with COPD and induced by cigarette smoke[J].Thorax, 2013, 68(5):410-420.
[14] ZHOU M, MENG L, HE Q, et al.Valsartan attenuates LPS-induced ALI by modulating NF-κB and MAPK pathways.[J].Front Pharmacol, 2024, 15: 1321095.
[15] ISSHIKI T, NAIEL S, VIERHOUT M, et al. Therapeutic strategies to target connective tissue growth factor in fibrotic lung diseases.[J].Pharmacol Ther, 2024, 253: 108578.
[16] ZHAO M, WANG M, CHEN X, et al. Targeting progranulin alleviated silica particles-induced pulmonary inflammation and fibrosis via decreasing Il-6 and Tgf-β1/Smad[J].J Hazard Mater, 2024, 465: 133199.
[17] YING H, FANG M, HANG Q Q, et al. Pirfenidone modulates macrophage polarization and ameliorates radiation-induced lung fibrosis by inhibiting the TGF-β1/Smad3 pathway[J]. J Cell Mol Med, 2021, 25: 8662-8675.
[18] XUX M, XU X H, CAO J L, et al. MicroRNA-1258 suppresses oxidative stress and inflammation in septic acute lungin jury through the Pknox1-regulated TGF-β1/SMAD3 cascade[J]. Clinics(SaoPaulo),2024,79:100354.

更新日期/Last Update: 2024-12-20