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Article ; Online: Fibroblast growth factor 21 attenuates ventilator-induced lung injury by inhibiting the NLRP3/caspase-1/GSDMD pyroptotic pathway.

Ding, Peng / Yang, Rui / Li, Cheng / Fu, Hai-Long / Ren, Guang-Li / Wang, Pei / Zheng, Dong-Yu / Chen, Wei / Yang, Li-Ye / Mao, Yan-Fei / Yuan, Hong-Bin / Li, Yong-Hua

Critical care (London, England)

2023 Volume 27, Issue 1, Page(s) 196

Abstract: Background: Ventilator-induced lung injury (VILI) is caused by overdistension of the alveoli by the repetitive recruitment and derecruitment of alveolar units. This study aims to investigate the potential role and mechanism of fibroblast growth factor ... ...

Abstract	Background: Ventilator-induced lung injury (VILI) is caused by overdistension of the alveoli by the repetitive recruitment and derecruitment of alveolar units. This study aims to investigate the potential role and mechanism of fibroblast growth factor 21 (FGF21), a metabolic regulator secreted by the liver, in VILI development. Methods: Serum FGF21 concentrations were determined in patients undergoing mechanical ventilation during general anesthesia and in a mouse VILI model. Lung injury was compared between FGF21-knockout (KO) mice and wild-type (WT) mice. Recombinant FGF21 was administrated in vivo and in vitro to determine its therapeutic effect. Results: Serum FGF21 levels in patients and mice with VILI were significantly higher than in those without VILI. Additionally, the increment of serum FGF21 in anesthesia patients was positively correlated with the duration of ventilation. VILI was aggravated in FGF21-KO mice compared with WT mice. Conversely, the administration of FGF21 alleviated VILI in both mouse and cell models. FGF21 reduced Caspase-1 activity, suppressed the mRNA levels of Nlrp3, Asc, Il-1β, Il-18, Hmgb1 and Nf-κb, and decreased the protein levels of NLRP3, ASC, IL-1β, IL-18, HMGB1 and the cleaved form of GSDMD. Conclusions: Our findings reveal that endogenous FGF21 signaling is triggered in response to VILI, which protects against VILI by inhibiting the NLRP3/Caspase-1/GSDMD pyroptosis pathway. These results suggest that boosting endogenous FGF21 or the administration of recombinant FGF21 could be promising therapeutic strategies for the treatment of VILI during anesthesia or critical care.
MeSH term(s)	Animals ; Mice ; Caspase 1/metabolism ; Disease Models, Animal ; HMGB1 Protein ; Inflammasomes ; Interleukin-18 ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Ventilator-Induced Lung Injury/drug therapy ; Ventilator-Induced Lung Injury/prevention & control ; Humans
Chemical Substances	Caspase 1 (EC 3.4.22.36) ; fibroblast growth factor 21 ; HMGB1 Protein ; Inflammasomes ; Interleukin-18 ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse
Language	English
Publishing date	2023-05-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2041406-7
ISSN	1466-609X ; 1364-8535
ISSN (online)	1466-609X
ISSN	1364-8535
DOI	10.1186/s13054-023-04488-5
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Zs.A 5517: Show issues

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Article ; Online: Elevated angiotensin II induces platelet apoptosis through promoting oxidative stress in an AT1R-dependent manner during sepsis.

Xu, Dun-Feng / Liu, Yu-Jian / Mao, Yan-Fei / Wang, Yan / Xu, Chu-Fan / Zhu, Xiao-Yan / Jiang, Lai

Journal of cellular and molecular medicine

2021 Volume 25, Issue 8, Page(s) 4124–4135

Abstract: Thrombocytopenia is independently related with increased mortality in severe septic patients. Renin-angiotensin system (RAS) is elevated in septic subjects; accumulating studies show that angiotensin II (Ang II) stimulate the intrinsic apoptosis pathway ... ...

Abstract	Thrombocytopenia is independently related with increased mortality in severe septic patients. Renin-angiotensin system (RAS) is elevated in septic subjects; accumulating studies show that angiotensin II (Ang II) stimulate the intrinsic apoptosis pathway by promoting reactive oxygen species (ROS) production. However, the mechanisms underlying the relationship of platelet apoptosis and RAS system in sepsis have not been fully elucidated. The present study aimed to elucidate whether the RAS was involved in the pathogenesis of sepsis-associated thrombocytopenia and explore the underlying mechanisms. We found that elevated plasma Ang II was associated with decreased platelet count in both patients with sepsis and experimental animals exposed to lipopolysaccharide (LPS). Besides, Ang II treatment induced platelet apoptosis in a concentration-dependent manner in primary isolated platelets, which was blocked by angiotensin II type 1 receptor (AT1R) antagonist losartan, but not by angiotensin II type 2 receptor (AT2R) antagonist PD123319. Moreover, inhibiting AT1R by losartan attenuated LPS-induced platelet apoptosis and alleviated sepsis-associated thrombocytopenia. Furthermore, Ang II treatment induced oxidative stress level in a concentration-dependent manner in primary isolated platelets, which was partially reversed by the AT1R antagonist losartan. The present study demonstrated that elevated Ang II directly stimulated platelet apoptosis through promoting oxidative stress in an AT1R-dependent manner in sepsis-associated thrombocytopenia. The results would helpful for understanding the role of RAS system in sepsis-associated thrombocytopenia.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Angiotensin II/pharmacology ; Angiotensin II Type 1 Receptor Blockers/pharmacology ; Animals ; Apoptosis ; Blood Platelets/drug effects ; Blood Platelets/metabolism ; Blood Platelets/pathology ; Case-Control Studies ; Cell Proliferation ; Cells, Cultured ; Female ; Gene Expression Regulation ; Humans ; Male ; Mice ; Middle Aged ; Oxidative Stress ; Prognosis ; Reactive Oxygen Species/metabolism ; Receptor, Angiotensin, Type 1/chemistry ; Receptor, Angiotensin, Type 1/genetics ; Receptor, Angiotensin, Type 1/metabolism ; Sepsis/complications ; Signal Transduction ; Thrombocytopenia/etiology ; Thrombocytopenia/metabolism ; Thrombocytopenia/pathology
Chemical Substances	Angiotensin II Type 1 Receptor Blockers ; Reactive Oxygen Species ; Receptor, Angiotensin, Type 1 ; Angiotensin II (11128-99-7)
Language	English
Publishing date	2021-02-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.16382
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Zs.A 5752: Show issues

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Article ; Online: DRD1 downregulation contributes to mechanical stretch-induced lung endothelial barrier dysfunction.

Wang, Yan / Liu, Yu-Jian / Xu, Dun-Feng / Zhang, Hui / Xu, Chu-Fan / Mao, Yan-Fei / Lv, Zhou / Zhu, Xiao-Yan / Jiang, Lai

Theranostics

2021 Volume 11, Issue 6, Page(s) 2505–2521

Abstract: Rationale: ...

Abstract	Rationale:
Language	English
Publishing date	2021-01-01
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.46192
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Article ; Online: Downregulation of R-Spondin1 Contributes to Mechanical Stretch-Induced Lung Injury.

Xu, Chu-Fan / Liu, Yu-Jian / Wang, Yan / Mao, Yan-Fei / Xu, Dun-Feng / Dong, Wen-Wen / Zhu, Xiao-Yan / Jiang, Lai

Critical care medicine

2019 Volume 47, Issue 7, Page(s) e587–e596

Abstract: Objectives: The R-spondin family attenuates tissue damage via tightening endothelium and preventing vascular leakage. This study aims to investigate whether R-spondins protect against mechanical stretch-induced endothelial dysfunction and lung injury ... ...

Abstract	Objectives: The R-spondin family attenuates tissue damage via tightening endothelium and preventing vascular leakage. This study aims to investigate whether R-spondins protect against mechanical stretch-induced endothelial dysfunction and lung injury and to reveal the underlying mechanisms. Design: Randomized controlled study. Setting: University research laboratory. Subjects: Patients scheduled to undergo surgery with mechanical ventilation support. Adult male Institute of Cancer Research mice. Primary cultured mouse lung vascular endothelial cells. Interventions: Patients underwent a surgical procedure with mechanical ventilation support of 3 hours or more. Mice were subjected to mechanical ventilation (6 or 30 mL/kg) for 0.5-4 hours. Another group of mice were intraperitoneally injected with 1 mg/kg lipopolysaccharide, and 12 hours later subjected to mechanical ventilation (10 mL/kg) for 4 hours. Mouse lung vascular endothelial cells were subjected to cyclic stretch for 4 hours. Measurements and main results: R-spondin1 were downregulated in both surgical patients and experimental animals exposed to mechanical ventilation. Intratracheal instillation of R-spondin1 attenuated, whereas knockdown of pulmonary R-spondin1 exacerbated ventilator-induced lung injury and mechanical stretch-induced lung vascular endothelial cell apoptosis. The antiapoptotic effect of R-spondin1 was mediated through the leucine-rich repeat containing G-protein coupled receptor 5 in cyclic stretched mouse lung vascular endothelial cells. We identified apoptosis-stimulating protein of p53 2 as the intracellular signaling protein interacted with leucine-rich repeat containing G-protein coupled receptor 5. R-spondin1 treatment decreased the interaction of apoptosis-stimulating protein of p53 2 with p53 while increased the binding of apoptosis-stimulating protein of p53 2 to leucine-rich repeat containing G-protein coupled receptor 5, therefore resulting in inactivation of p53-mediated proapoptotic pathway in cyclic stretched mouse lung vascular endothelial cells. Conclusions: Mechanical ventilation leads to down-regulation of R-spondin1. R-spondin1 may enhance the interaction of leucine-rich repeat containing G-protein coupled receptor 5 and apoptosis-stimulating protein of p53 2, thus inactivating p53-mediated proapoptotic pathway in cyclic stretched mouse lung vascular endothelial cells. R-spondin1 may have clinical benefit in alleviating mechanical ventilator-induced lung injury.
MeSH term(s)	Animals ; Male ; Mice ; Bronchoalveolar Lavage Fluid/cytology ; Cells, Cultured ; Disease Models, Animal ; Down-Regulation/physiology ; Lung/physiopathology ; Random Allocation ; Real-Time Polymerase Chain Reaction ; Signal Transduction ; Thrombospondins/blood ; Ventilator-Induced Lung Injury/prevention & control ; Humans
Chemical Substances	Thrombospondins ; RSPO1 protein, human
Language	English
Publishing date	2019-06-07
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	197890-1
ISSN	1530-0293 ; 0090-3493
ISSN (online)	1530-0293
ISSN	0090-3493
DOI	10.1097/CCM.0000000000003767
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Zs.A 1261: Show issues

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Article ; Online: Upregulation of Matrix Metalloproteinase-9 Protects against Sepsis-Induced Acute Lung Injury via Promoting the Release of Soluble Receptor for Advanced Glycation End Products.

Zhang, Hui / Mao, Yan-Fei / Zhao, Ying / Xu, Dun-Feng / Wang, Yan / Xu, Chu-Fan / Dong, Wen-Wen / Zhu, Xiao-Yan / Ding, Ning / Jiang, Lai / Liu, Yu-Jian

Oxidative medicine and cellular longevity

2021 Volume 2021, Page(s) 8889313

Abstract: Dysregulation of matrix metalloproteinase- (MMP-) 9 is implicated in the pathogenesis of acute lung injury (ALI). However, it remains controversial whether MMP-9 improves or deteriorates acute lung injury of different etiologies. The receptor for ... ...

Abstract	Dysregulation of matrix metalloproteinase- (MMP-) 9 is implicated in the pathogenesis of acute lung injury (ALI). However, it remains controversial whether MMP-9 improves or deteriorates acute lung injury of different etiologies. The receptor for advanced glycation end products (RAGE) plays a critical role in the pathogenesis of acute lung injury. MMPs are known to mediate RAGE shedding and release of soluble RAGE (sRAGE), which can act as a decoy receptor by competitively inhibiting the binding of RAGE ligands to RAGE. Therefore, this study is aimed at clarifying whether and how pulmonary knockdown of MMP-9 affected sepsis-induced acute lung injury as well as the release of sRAGE in a murine cecal ligation and puncture (CLP) model. The analysis of GEO mouse sepsis datasets GSE15379, GSE52474, and GSE60088 revealed that the mRNA expression of MMP-9 was significantly upregulated in septic mouse lung tissues. Elevation of pulmonary MMP-9 mRNA and protein expressions was confirmed in CLP-induced mouse sepsis model. Intratracheal injection of MMP-9 siRNA resulted in an approximately 60% decrease in pulmonary MMP-9 expression. It was found that pulmonary knockdown of MMP-9 significantly increased mortality of sepsis and exacerbated sepsis-associated acute lung injury. Pulmonary MMP-9 knockdown also decreased sRAGE release and enhanced sepsis-induced activation of the RAGE/nuclear factor-
MeSH term(s)	Acute Lung Injury/etiology ; Animals ; Cecum ; Disease Models, Animal ; Gene Knockdown Techniques ; Inflammation/pathology ; Ligation ; Lung/pathology ; Male ; Matrix Metalloproteinase 9/metabolism ; Mice, Inbred ICR ; NF-kappa B/metabolism ; Punctures ; Receptor for Advanced Glycation End Products/metabolism ; Sepsis/complications ; Signal Transduction ; Solubility ; Up-Regulation ; Mice
Chemical Substances	NF-kappa B ; Receptor for Advanced Glycation End Products ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2021-02-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2021/8889313
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Article ; Online: Salidroside Attenuates Ventilation Induced Lung Injury via SIRT1-Dependent Inhibition of NLRP3 Inflammasome.

Wang, Yan / Xu, Chu-Fan / Liu, Yu-Jian / Mao, Yan-Fei / Lv, Zhou / Li, Si-Yuan / Zhu, Xiao-Yan / Jiang, Lai

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2017 Volume 42, Issue 1, Page(s) 34–43

Abstract: Background: Salidroside (SDS) is the main effective ingredient of Rhodiola rosea L with a variety of pharmacologic properties. We aim to investigate the effects of SDS on ventilation induced lung injury (VILI) and explore the possible underlying ... ...

Abstract	Background: Salidroside (SDS) is the main effective ingredient of Rhodiola rosea L with a variety of pharmacologic properties. We aim to investigate the effects of SDS on ventilation induced lung injury (VILI) and explore the possible underlying molecular mechanism. Methods: Lung injury was induced in male ICR mice via mechanical ventilation (30 ml/kg) for 4h. The mice were divided in four groups:(1) Control group; (2) Ventilation group; (3) SDS group; (4) Ventilation with SDS group. SDS (50 mg/kg) was injected intraperitoneally 1h before operation. Mouse lung vascular endothelial cells (MLVECs) were subjected to cyclic stretch for 4h. Results: It was found that SDS attenuated VILI as shown in HE staining, cell count and protein content levels in BAL fluid, W/D and Evans blue dye leakage into the lung tissue. SDS treatment inhibited the activation of NLRP3 inflammasome and subsequent caspase-1 cleavage as well as interleukin (IL)-1β secretion both in vivo and in vitro. Moreover, SDS administration up-regulated SIRT1 expression. Importantly, knockdown of SIRT1 reversed the inhibitory effect of SDS on NLRP3 inflammasome activation. Conclusions: Taken together, these findings indicate that SDS may confer protection against ventilation induced lung injury via SIRT1-de-pendent inhibition of NLRP3 inflammasome activation.
MeSH term(s)	Animals ; Bronchoalveolar Lavage Fluid/chemistry ; Caspase 1/metabolism ; Cells, Cultured ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Enzyme-Linked Immunosorbent Assay ; Glucosides/pharmacology ; Glucosides/therapeutic use ; Inflammasomes/metabolism ; Interleukin-1beta/analysis ; Interleukin-1beta/metabolism ; Lung/metabolism ; Lung/pathology ; Male ; Mice ; Mice, Inbred ICR ; NLR Family, Pyrin Domain-Containing 3 Protein/antagonists & inhibitors ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Phenols/pharmacology ; Phenols/therapeutic use ; RNA Interference ; RNA, Small Interfering/metabolism ; Sirtuin 1/antagonists & inhibitors ; Sirtuin 1/genetics ; Sirtuin 1/metabolism ; Stress, Mechanical ; Up-Regulation/drug effects ; Ventilator-Induced Lung Injury/metabolism ; Ventilator-Induced Lung Injury/pathology ; Ventilator-Induced Lung Injury/prevention & control
Chemical Substances	Glucosides ; Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Phenols ; RNA, Small Interfering ; Caspase 1 (EC 3.4.22.36) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; rhodioloside (M983H6N1S9)
Language	English
Publishing date	2017-05-10
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000477112
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Zs.A 3160: Show issues

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Article ; Online: Protective Effects of Hydrogen-Rich Saline Against Lipopolysaccharide-Induced Alveolar Epithelial-to-Mesenchymal Transition and Pulmonary Fibrosis.

Dong, Wen-Wen / Zhang, Yun-Qian / Zhu, Xiao-Yan / Mao, Yan-Fei / Sun, Xue-Jun / Liu, Yu-Jian / Jiang, Lai

Medical science monitor : international medical journal of experimental and clinical research

2017 Volume 23, Page(s) 2357–2364

Abstract: BACKGROUND Fibrotic change is one of the important reasons for the poor prognosis of patients with acute respiratory distress syndrome (ARDS). The present study investigated the effects of hydrogen-rich saline, a selective hydroxyl radical scavenger, on ... ...

Abstract	BACKGROUND Fibrotic change is one of the important reasons for the poor prognosis of patients with acute respiratory distress syndrome (ARDS). The present study investigated the effects of hydrogen-rich saline, a selective hydroxyl radical scavenger, on lipopolysaccharide (LPS)-induced pulmonary fibrosis. MATERIAL AND METHODS Male ICR mice were divided randomly into 5 groups: Control, LPS-treated plus vehicle treatment, and LPS-treated plus hydrogen-rich saline (2.5, 5, or 10 ml/kg) treatment. Twenty-eight days later, fibrosis was assessed by determination of collagen deposition, hydroxyproline, and type I collagen levels. Development of epithelial-to-mesenchymal transition (EMT) was identified by examining protein expressions of E-cadherin and α-smooth muscle actin (α-SMA). Transforming growth factor (TGF)-β1 content, total antioxidant capacity (T-AOC), malondialdehyde (MDA) content, catalase (CAT), and superoxide dismutase (SOD) activity were determined. RESULTS Mice exhibited increases in collagen deposition, hydroxyproline, type I collagen contents, and TGF-β1 production in lung tissues after LPS treatment. LPS-induced lung fibrosis was associated with increased expression of α-SMA, as well as decreased expression of E-cadherin. In addition, LPS treatment increased MDA levels but decreased T-AOC, CAT, and SOD activities in lung tissues, indicating that LPS induced pulmonary oxidative stress. Hydrogen-rich saline treatment at doses of 2.5, 5, or 10 ml/kg significantly attenuated LPS-induced pulmonary fibrosis. LPS-induced loss of E-cadherin in lung tissues was largely reversed, whereas the acquisition of α-SMA was dramatically decreased by hydrogen-rich saline treatment. In addition, hydrogen-rich saline treatment significantly attenuated LPS-induced oxidative stress. CONCLUSIONS Hydrogen-rich saline may protect against LPS-induced EMT and pulmonary fibrosis through suppressing oxidative stress.
MeSH term(s)	Animals ; Cadherins/metabolism ; Collagen/metabolism ; Collagen Type I/metabolism ; Epithelial Cells/metabolism ; Epithelial-Mesenchymal Transition/drug effects ; Fibrosis ; Hydrogen/therapeutic use ; Hydroxyproline/metabolism ; Lipopolysaccharides ; Lung/pathology ; Male ; Mice ; Mice, Inbred ICR ; Oxidative Stress/drug effects ; Pulmonary Fibrosis/prevention & control ; Pulmonary Fibrosis/therapy ; Respiratory Distress Syndrome, Adult/therapy ; Sodium Chloride/therapeutic use ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Cadherins ; Collagen Type I ; Lipopolysaccharides ; Transforming Growth Factor beta1 ; Sodium Chloride (451W47IQ8X) ; Hydrogen (7YNJ3PO35Z) ; Collagen (9007-34-5) ; Hydroxyproline (RMB44WO89X)
Language	English
Publishing date	2017-05-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	1439041-3
ISSN	1643-3750 ; 1234-1010
ISSN (online)	1643-3750
ISSN	1234-1010
DOI	10.12659/msm.900452
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Zs.A 4924: Show issues

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Article: Interleukin-35 Attenuates D-Galactosamine/Lipopolysaccharide-Induced Liver Injury via Enhancing Interleukin-10 Production in Kupffer Cells.

Zheng, Xing-Feng / Hu, Xiao-Yan / Ma, Bing / Fang, He / Zhang, Fang / Mao, Yan-Fei / Yang, Feng-Yong / Xiao, Shi-Chu / Xia, Zhao-Fan

Frontiers in pharmacology

2018 Volume 9, Page(s) 959

Abstract: Interleukin (IL) -35 is an anti-inflammatory cytokine which exerts various beneficial effects on autoimmune diseases. However, whether IL-35 plays a role in endotoxin induced hepatitis demands clarification. This study aims to reveal the effect and ... ...

Abstract	Interleukin (IL) -35 is an anti-inflammatory cytokine which exerts various beneficial effects on autoimmune diseases. However, whether IL-35 plays a role in endotoxin induced hepatitis demands clarification. This study aims to reveal the effect and mechanism of IL-35 on endotoxin induced liver injury. Acute hepatic injury was induced by D-galactosamine (D-GalN, 400 mg/kg) and lipopolysaccharide (LPS, 5 μg/kg) administration in mice. IL-35 treatment ameliorated D-GalN/LPS induced liver injury in a dose dependent manner as shown by histological examination, ALT determination and Caspase-3 activity assay. It also reduced production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, IL-1β, and IL-6, and increased production of anti-inflammatory cytokines, IL-4, IL-10, and transforming growth factor (TGF)-β. This hepato-protective effect was proved mainly mediated by Kupffer cells (KC) via gadolinium chloride depletion and cell adoptive transfer experiment. In addition, IL-35 emolliated the cytotoxicity of LPS-triggered KCs to hepatocytes, suppressed nitric oxide (NO) and TNF-α production, and elevated IL-10 production in LPS stimulated KCs. Furthermore, IL-35 could not exert hepato-protective effect in IL-10-deficient mice
Language	English
Publishing date	2018-08-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2018.00959
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Article ; Online: Resveratrol ameliorates lipopolysaccharide-induced epithelial mesenchymal transition and pulmonary fibrosis through suppression of oxidative stress and transforming growth factor-β1 signaling.

Zhang, Yun-Qian / Liu, Yu-Jian / Mao, Yan-Fei / Dong, Wen-Wen / Zhu, Xiao-Yan / Jiang, Lai

Clinical nutrition (Edinburgh, Scotland)

2015 Volume 34, Issue 4, Page(s) 752–760

Abstract: Background & aims: Fibrotic changes seem to be responsible for the high mortality rate observed in patients with acute respiratory distress syndrome (ARDS). The present study aimed to determine whether resveratrol, a natural antioxidant polyphenol, had ... ...

Abstract	Background & aims: Fibrotic changes seem to be responsible for the high mortality rate observed in patients with acute respiratory distress syndrome (ARDS). The present study aimed to determine whether resveratrol, a natural antioxidant polyphenol, had anti-fibrotic effects in the murine model of lipopolysaccharide (LPS)-induced pulmonary fibrosis. Methods: Fibrosis was assessed by determination of collagen deposition, hydroxyproline and type I collagen levels in lung tissues. Development of epithelial-mesenchymal transition (EMT) was identified by the loss of E-cadherin accompanying by the acquisition of α-smooth muscle actin (α-SMA). Transforming growth factor (TGF)-β1 content, levels of phosphorylated Smad2/Smad3 and Smad4, malondialdehyde (MDA) content, total antioxidant capacity (T-AOC), superoxide dismutase (SOD) activity, and catalase (CAT) activity in lung tissues were determined. Results: LPS increased collagen deposition, hydroxyproline and type I collagen contents, and meanwhile induced EMT process, stimulated TGF-β1 production and Smad activation in lung tissues on day 21 to day 28 after LPS administration. In addition, LPS treatment resulted in a rapid induction of oxidative stress as evidenced by increase of MDA and decreases of T-AOC, CAT and SOD activities as early as 7 days after LPS treatment, which was persistent for at least 4 weeks. In contrast, resveratrol treatment attenuated LPS-induced EMT and pulmonary fibrosis, meanwhile it suppressed LPS-induced oxidative stress, TGF-β1 production and activation of Smad signaling pathway. Conclusions: Resveratrol may ameliorate LPS-induced EMT and pulmonary fibrosis through suppression of oxidative stress and TGF-β1/Smad signaling pathway. Application of antioxidants may represent a useful adjuvant pharmacologic approach to reduce ARDS-associated pulmonary fibrosis.
MeSH term(s)	Animals ; Catalase/metabolism ; Collagen Type I/metabolism ; Disease Models, Animal ; Epithelial-Mesenchymal Transition/drug effects ; Lipopolysaccharides/adverse effects ; Male ; Malondialdehyde/metabolism ; Mice ; Mice, Inbred ICR ; Oxidative Stress/drug effects ; Pulmonary Fibrosis/chemically induced ; Pulmonary Fibrosis/drug therapy ; Signal Transduction ; Stilbenes/pharmacology ; Superoxide Dismutase/metabolism ; Transforming Growth Factor beta1/genetics ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Collagen Type I ; Lipopolysaccharides ; Stilbenes ; Transforming Growth Factor beta1 ; Malondialdehyde (4Y8F71G49Q) ; Catalase (EC 1.11.1.6) ; Superoxide Dismutase (EC 1.15.1.1) ; resveratrol (Q369O8926L)
Language	English
Publishing date	2015-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604812-2
ISSN	1532-1983 ; 0261-5614
ISSN (online)	1532-1983
ISSN	0261-5614
DOI	10.1016/j.clnu.2014.08.014
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Zs.A 1774: Show issues

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Article ; Online: Lung endothelial barrier protection by resveratrol involves inhibition of HMGB1 release and HMGB1-induced mitochondrial oxidative damage via an Nrf2-dependent mechanism.

Dong, Wen-Wen / Liu, Yu-Jian / Lv, Zhou / Mao, Yan-Fei / Wang, Ying-Wei / Zhu, Xiao-Yan / Jiang, Lai

Free radical biology & medicine

2015 Volume 88, Issue Pt B, Page(s) 404–416

Abstract: High-mobility group box 1 (HMGB1) contributes to lung vascular hyperpermeability during ventilator-induced lung injury. We aimed to determine whether the natural antioxidant resveratrol protected against HMGB1-induced endothelial hyperpermeability both ... ...

Abstract	High-mobility group box 1 (HMGB1) contributes to lung vascular hyperpermeability during ventilator-induced lung injury. We aimed to determine whether the natural antioxidant resveratrol protected against HMGB1-induced endothelial hyperpermeability both in vitro and in vivo. We found that HMGB1 decreased vascular endothelial (VE)-cadherin expression and increased endothelial permeability, leading to mitochondrial oxidative damage in primary cultured mouse lung vascular endothelial cells (MLVECs). Both the mitochondrial superoxide dismutase 2 mimetic MnTBAP and resveratrol blocked HMGB1-induced mitochondrial oxidative damage, VE-cadherin downregulation, and endothelial hyperpermeability. In in vivo studies, anesthetized male ICR mice were ventilated for 4h using low tidal volume (6 ml/kg) or high tidal volume (HVT; 30 ml/kg) ventilation. The mice were injected intraperitoneally with resveratrol immediately before the onset of ventilation. We found that resveratrol attenuated HVT-associated lung vascular hyperpermeability and HMGB1 production. HVT caused a significant increase in nuclear factor-erythroid 2-related factor 2 (Nrf2) nuclear translocation and Nrf2 target gene expression in lung tissues, which was further enhanced by resveratrol treatment. HMGB1 had no effect on Nrf2 activation, whereas resveratrol treatment activated the Nrf2 signaling pathway in HMGB1-treated MLVECs. Moreover, Nrf2 knockdown reversed the inhibitory effects of resveratrol on HMGB1-induced mitochondrial oxidative damage and endothelial hyperpermeability. The inhibitory effect of resveratrol on cyclic stretch-induced HMGB1 mRNA expression in primary cultured MLVECs was also abolished by Nrf2 knockdown. In summary, this study demonstrates that resveratrol protects against lung endothelial barrier dysfunction initiated by HVT. Lung endothelial barrier protection by resveratrol involves inhibition of mechanical stretch-induced HMGB1 release and HMGB1-induced mitochondrial oxidative damage. These protective effects of resveratrol might be mediated through an Nrf2-dependent mechanism.
MeSH term(s)	Animals ; Antioxidants/pharmacology ; Blotting, Western ; Disease Models, Animal ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Fluorescent Antibody Technique ; Gene Knockdown Techniques ; HMGB1 Protein/metabolism ; Lung/drug effects ; Lung/metabolism ; Lung/pathology ; Male ; Mice ; Mice, Inbred ICR ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; RNA, Small Interfering ; Real-Time Polymerase Chain Reaction ; Stilbenes/pharmacology ; Stress, Mechanical ; Transfection ; Ventilator-Induced Lung Injury/metabolism ; Ventilator-Induced Lung Injury/physiopathology
Chemical Substances	Antioxidants ; HMGB1 Protein ; NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse ; RNA, Small Interfering ; Stilbenes ; resveratrol (Q369O8926L)
Language	English
Publishing date	2015-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2015.05.004
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