hucMSC Conditioned Medium Ameliorate Lipopolysaccharide-Induced Acute Lung Injury by Suppressing Oxidative Stress and Inflammation via Nrf2/NF-κB Signaling Pathway.
hucMSC Conditioned Medium Ameliorate Lipopolysaccharide-Induced Acute Lung Injury by Suppressing Oxidative Stress and Inflammation via Nrf2/NF-κB Signaling Pathway.
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HucMSC 条件培养基通过 Nrf2/NF-κB 信号通路抑制氧化应激和炎症，改善脂多糖引起的急性肺损伤
DOI：
10.1155/2021/6653681
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Liu B
中科院分区：
文献类型：
--
作者：
Tang Y;Ding F;Wu C;Liu B
急性肺损伤（acute lung injury，ALI）是心脏重症监护病房常见的临床综合征，病死率高。炎症和氧化应激在ALI的发生发展中起着重要作用。已有研究表明，人脐带间充质干细胞（human umbilical cord mesenchymal stem cells，hucMSCs）在多种疾病中具有抗炎和抗氧化作用。然而，hucMSC条件培养基（CM）对LPS诱导的ALI的抗炎和抗氧化作用仍不清楚。因此，在这项研究中，我们评估了hucMSC条件培养基是否可以减轻LPS诱导的ALI及其潜在机制。将小鼠随机分为4组：对照组、PBS组、LPS+PBS组、LPS+CM组。干预后行肺组织病理学及支气管肺泡灌洗液（BALF）分析。检测Nrf 2/NF-κB信号通路及其下游靶基因，并检测CM中细胞因子和生长因子的含量。结果表明，CM可显著减轻组织学改变，降低湿/干重比，降低MPO、MDA和ROS水平，提高SOD和GSH活性，下调IL-1β、IL-6和TNF-α等促炎细胞因子水平。CM还可促进Nrf 2及其靶基因NQ 01、HO-1和GCLC的表达，抑制NF-κB B及其靶基因IL-6、IL-1β和TNF-α的表达。这些作用可能与CM中大量的细胞因子和生长因子密切相关。结论：CM可减轻LPS诱导的ALI，其机制可能与抑制炎症反应和氧化应激有关，其机制可能与抑制Nrf 2/NF-κB信号通路有关。
Acute lung injury (ALI) is a common clinical syndrome in the cardiac intensive care unit with a high mortality rate. Inflammation and oxidative stress have been reported to play a crucial role in the development of ALI. Previous studies have shown that human umbilical cord mesenchymal stem cells (hucMSCs) have anti-inflammatory and antioxidative effects in various diseases. However, the anti-inflammatory and antioxidative effects of the hucMSC conditioned medium (CM) on LPS-induced ALI remain unclear. Therefore, in this study, we assessed whether the hucMSC conditioned medium could attenuate LPS-induced ALI and the underlying mechanisms. Mice were randomly divided into four groups: the control group, PBS group, LPS+PBS group, and LPS+CM group. The lung histopathology and bronchoalveolar lavage fluid (BALF) were analyzed after intervention. The Nrf2/NF-κB signaling pathway and its downstream target genes were tested, and the cytokines and growth factors in CM were also measured. The results showed that CM significantly attenuated the histological alterations; decreased the wet/dry weight ratio; reduced the levels of MPO, MDA and ROS; increased SOD and GSH activity; and downregulated the level of proinflammatory cytokines such as IL-1β, IL-6, and TNF-α. Furthermore, CM promoted the expression of Nrf2 and its target genes NQ01, HO-1, and GCLC and inhibited the expression of NF-κB and its target genes IL-6, IL-1β, and TNF-α. These effects may be closely related to the large amounts of cytokines and growth factors in the CM. In conclusion, our results demonstrated that CM could attenuate LPS-induced ALI, probably due to inhibition of inflammation and oxidative stress via the Nrf2/NF-κB signaling pathway.
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影响因子：
5.6
作者：
Sun, Xue-qian;Wu, Chen;Pang, Qing-feng
通讯作者：
Pang, Qing-feng
DOI：
10.1152/ajplung.00281.2016
发表时间：
2016-11-01
影响因子：
4.9
作者：
Zhao, Jiping;Yu, Hao;Qin, Hongwei
通讯作者：
Qin, Hongwei
IRF-1 干预 LPS 诱导的小鼠急性肺损伤期间经典 ROS 依赖性 NET 释放
影响因子：
5.1
作者：
Liu, Shuai;Yue, Yinyan;Mao, Zhi
通讯作者：
Mao, Zhi
影响因子：
5.6
作者：
Leung, Wai-Shing;Yang, Ming-Ling;Kuan, Yu-Hsiang
通讯作者：
Kuan, Yu-Hsiang
影响因子：
7.5
作者：
Liu B;Ding F;Hu D;Zhou Y;Long C;Shen L;Zhang Y;Zhang D;Wei G
通讯作者：
Wei G