Biochanin A protect against lipopolysaccharide-induced acute lung injury in mice by regulating TLR4/NF-κB and PPAR-γ pathway

Xiansheng, Hu; Qin, Hongyu; Liu, Yunpeng; Li, Jingxian; Fu, Lianjun; Mu-sen, LI; Jiang, Cheng; Yun, Jinyan; Zhi-hu, Liu; Yao, Feng; Ying, Yang; Yin, Baoshu

doi:10.1016/j.micpath.2019.103846

Cited by 33 publications

(27 citation statements)

References 25 publications

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“…[ 40 ] In response to LPS challenge, these proinflammatory cytokines may activate lung epithelial cells to recruit the inflammatory cell into the lung, thus leading to severe ALI. [ 21 ] There is abundant evidence suggesting that stimulation of lung epithelial cells by LPS could induce TNF‐α, IL‐1β, and IL‐6 production. [ 41 ] In line with the inhibited infiltration of neutrophils and macrophages, TNF‐α, IL‐1β, and IL‐6 production was also downregulated in BALF of LPS‐treated mice pretreated with FA in a dose‐dependent manner.…”

Section: Discussionmentioning

confidence: 99%

“…[ 45 ] Increasing evidence has suggested that the inactivation of the TLR4/NF‐κB signaling pathway by some natural products could attenuate ALI in mice. [ 21,46 ] Hence, any drug focusing on blocking TLR4/NF‐κB signaling to attenuate inflammatory response would provide potential therapeutic effects for ALI. As expected, after LPS stimulation, the expression of TLR4, phosphorylation of NF‐κB p65, and phosphorylation of IκBα in the lung tissues were elevated in lung tissues.…”

Section: Discussionmentioning

confidence: 99%

“…After centrifugation (12,000 rpm, 10 min), the resulting supernatant of lung homogenates was collected and assayed for MPO activity and MCP‐1 level using the respective commercial ELISA assay kits following the manufacturer's instructions. [ 21 ]…”

Section: Methodsmentioning

confidence: 99%

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Ferulic acid alleviates lipopolysaccharide‐induced acute lung injury through inhibiting TLR4/NF‐κB signaling pathway

Lin

2020

J Biochem & Molecular Tox

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Ferulic acid (FA) exhibits anti‐inflammatory, antidiabetic, antihyperlipidemic, antioxidant, neuroprotective, and antihypertensive effects. This study aimed to determine whether FA could ameliorate lipopolysaccharide (LPS)‐induced inflammatory responses and acute lung injury (ALI) in mice. Mice were challenged with LPS intratracheally to induce ALI 1 h after 3 days of FA (25, 50, and 100 mg/kg) or dexamethasone (DEX; 5 mg/kg) administration. The lung tissues and bronchoalveolar lavage fluid (BALF) were collected 12 h after the LPS challenge. Pretreatment with FA or DEX could attenuate lung histopathological change, complement deposition, and lung wet‐to‐dry weight ratio of mice injured by LPS. Meanwhile, the influx of neutrophils and macrophages, as well as the production of proinflammatory cytokine (tumor necrosis factor‐alpha, interleukin 1 beta [IL‐1β], and IL‐6), in BALF of ALI mice was significantly decreased. Moreover, FA or DEX markedly reversed the LPS‐induced elevation of myeloperoxidase activity and monocyte chemoattractant protein‐1 level in lung tissues of ALI mice. In addition, the Western blot analysis demonstrated that FA or DEX effectively inhibited the LPS‐induced activation of the toll‐like receptor 4 (TLR4)/nuclear factor‐kappa B (NF‐κB) signaling pathway in lung tissues. The current study suggested that the alleviating effect of FA against LPS‐induced ALI might be partially due to the inhibition of the inflammatory response via inactivation of the TLR4/NF‐κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Ferulic acid alleviates lipopolysaccharide‐induced acute lung injury through inhibiting TLR4/NF‐κB signaling pathway

Lin

2020

J Biochem & Molecular Tox

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“…Activation of the PPAR γ /LXR α and PPAR γ /HO-1 pathways also contributes to prevention of inflammatory response in multiple cell types [ 16 , 34 ]. Given BCA as a positive regulator of PPAR γ expression [ 35 , 36 ], we inferred that the anti-inflammatory effect of BCA is mediated by these two signaling pathways. To do so, THP-1 macrophage-derived foam cells were pretreated with siRNAs against PPAR γ , LXR α , or HO-1, followed by incubation with or without BCA.…”

Section: Resultsmentioning

confidence: 99%

Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response

Chen

Deng

et al. 2020

Oxidative Medicine and Cellular Longevity

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Biochanin A (BCA), a dietary isoflavone extracted from red clover and cabbage, has been shown to antagonize hypertension and myocardial ischemia/reperfusion injury. However, very little is known about its role in atherogenesis. The aim of this study was to observe the effects of BCA on atherosclerosis and explore the underlying mechanisms. Our results showed that administration of BCA promoted reverse cholesterol transport (RCT), improved plasma lipid profile, and decreased serum proinflammatory cytokine levels and atherosclerotic lesion area in apoE-/- mice fed a Western diet. In THP-1 macrophage-derived foam cells, treatment with BCA upregulated ATP-binding cassette (ABC) transporter A1 (ABCA1) and ABCG1 expression and facilitated subsequent cholesterol efflux and diminished intracellular cholesterol contents by activating the peroxisome proliferator-activated receptor γ (PPARγ)/liver X receptor α (LXRα) and PPARγ/heme oxygenase 1 (HO-1) pathways. BCA also activated these two signaling pathways to inhibit the secretion of proinflammatory cytokines. Taken together, these findings suggest that BCA is protective against atherosclerosis by inhibiting lipid accumulation and inflammatory response through the PPARγ/LXRα and PPARγ/HO-1 pathways. BCA may be an attractive drug for the prevention and treatment of atherosclerotic cardiovascular disease.

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“…The glycoproteins of R. japonica var. glaucocalyx (XPS) were isolated from the aqueous extracts of this plant, and two homogeneous glycoproteins (XPS5-1 and XPS10-1) were purified from XPS (Wang et al, 2020a). Our previous research found that XPS5-1 and XPS10-1 had antitumor activity in vitro (Wang et al, 2020a) but their anti-inflammatory effect remained unclear.…”

Section: Introductionmentioning

confidence: 99%

Glycoproteins From Rabdosia japonica var. glaucocalyx Regulate Macrophage Polarization and Alleviate Lipopolysaccharide-Induced Acute Lung Injury in Mice via TLR4/NF-κB Pathway

et al. 2021

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Background and Aims:Rabdosia japonica var. glaucocalyx is a traditional Chinese medicine (TCM) for various inflammatory diseases. This present work aimed to investigate the protective effects of R. japonica var. glaucocalyx glycoproteins on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the potential mechanism.Methods: Glycoproteins (XPS) were isolated from R. japonica var. glaucocalyx, and homogeneous glycoprotein (XPS5-1) was purified from XPS. ANA-1 cells were used to observe the effect of glycoproteins on the secretion of inflammatory mediators by enzyme-linked immunosorbent assay (ELISA). Flow cytometry assay, immunofluorescence assay, and Western blot analysis were performed to detect macrophage polarization in vitro. The ALI model was induced by LPS via intratracheal instillation, and XPS (20, 40, and 80 mg/kg) was administered intragastrically 2 h later. The mechanisms of XPS against ALI were investigated by Western blot, ELISA, and immunohistochemistry.Results:In vitro, XPS and XPS5-1 downregulated LPS-induced proinflammatory mediators production including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and nitric oxide (NO) and upregulated LPS-induced IL-10 secretion. The LPS-stimulated macrophage polarization was also modulated from M1 to M2. In vivo, XPS maintained pulmonary histology with significantly reducing protein concentration and numbers of mononuclear cells in bronchoalveolar lavage fluid (BALF). The level of IL-10 in BALF was upregulated by XPS treatment. The level of cytokines including TNF-α, IL-1β, and IL-6 was downregulated. XPS also decreased infiltration of macrophages and polymorphonuclear leukocytes (PMNs) in lung. XPS suppressed the expression of key proteins in the TLR4/NF-κB signal pathway.Conclusion: XPS was demonstrated to be a potential agent for treating ALI. Our findings might provide evidence supporting the traditional application of R. japonica var. glaucocalyx in inflammation-linked diseases.

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Biochanin A protect against lipopolysaccharide-induced acute lung injury in mice by regulating TLR4/NF-κB and PPAR-γ pathway

Cited by 33 publications

References 25 publications

Ferulic acid alleviates lipopolysaccharide‐induced acute lung injury through inhibiting TLR4/NF‐κB signaling pathway

Ferulic acid alleviates lipopolysaccharide‐induced acute lung injury through inhibiting TLR4/NF‐κB signaling pathway

Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response

Glycoproteins From Rabdosia japonica var. glaucocalyx Regulate Macrophage Polarization and Alleviate Lipopolysaccharide-Induced Acute Lung Injury in Mice via TLR4/NF-κB Pathway

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