Low molecular weight fucoidan attenuating pulmonary fibrosis by relieving inflammatory reaction and progression of epithelial-mesenchymal transition

Wu, Ning; Li, Zhi; Wang, Jing; Geng, Lihua; Yue, Yang; Deng, Zhenzhen; Wang, Qingchi; Zhang, Quanbin

doi:10.1016/j.carbpol.2021.118567

Cited by 32 publications

(25 citation statements)

References 46 publications

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“…Mounting evidence revealed that PI3K/Akt signaling-mediated-in ammation may be responsible for various brosis diseases, including lung brosis [31,55,56], liver brosis [57], and intestinal brosis [58]. Therefore, inactivation of PI3K/Akt pathway attenuated PF progression via relieving in ammation and progression of EMT [59]. Consistently, the study on the anti-PF effects of Qingfei Paidu decoction (QFPD), a well-known Chinese herbal formula for the management of patients diagnosed with COVID-19, also indicated that QFPD can effectively alleviate the BLM-induced in ammation and collagen deposition in mice [60].…”

Section: Discussionmentioning

confidence: 99%

Investigation of Anti-Epithelial-Mesenchymal Transition and Anti-Inflammation effects of Qing Fei Hua Xian Decotion on Pulmonary Fibrosis via Network Pharmacology and Experimental Verification

Wang

et al. 2022

Preprint

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Background Pulmonary fibrosis (PF) is a common interstitial pneumonia disease, also occurred in post-COVID-19 survivors. The mechanism underlying the anti-PF effect of Qing Fei Hua Xian Decotion (QFHXD), a traditional Chinese medicine formula applied for treating PF in COVID-19 survivors, is unclear. This study aimed to uncover the mechanisms related to the anti-PF effect of QFHXD through analysis of network pharmacology and experimental verification. Methods The candidate chemical compounds of QFHXD and its putative targets for treating PF were achieved from public databases, thereby we established the corresponding “herb- compound -target” network of QFHXD. Moreover, The protein–protein interaction (PPI) network of potential targets was also constructed to screen the core targets. Furthermore, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were used to predict targets, and pathways, then validated by in vivo experiments. Results A total of 188 active compounds in QFHXD and 50 target genes were identified from databases. The key therapeutic targets of QFHXD, such as PI3K/Akt, IL-6, TNF, IL-1β, STAT3, MMP-9, and TGF-β1 were identified by KEGG and GO analysis. Anti-PF effects of QFHXD (in a dose-dependent manner) and prednisone were confirmed by HE, Masson staining, and Sirius red staining as well as in vivo Micro-CT and immunohistochemical analysis in a rat model of bleomycin-induced PF. Besides, QFXHD remarkably inhibits the activity of PI3K/Akt/NF-κB and TGF‑β1/Smad2/3. Conclusion QFXHD significantly attenuated bleomycin-induced PF via inhibiting inflammation and EMT. PI3K/Akt/NF-κB and TGF‑β1/Smad2/3 pathways might be the potential therapeutic effects of QFHXD for treating PF.

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Section: Discussionmentioning

confidence: 99%

Investigation of Anti-Epithelial-Mesenchymal Transition and Anti-Inflammation effects of Qing Fei Hua Xian Decotion on Pulmonary Fibrosis via Network Pharmacology and Experimental Verification

Wang

et al. 2022

Preprint

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“…[29,32,55] Mechanistically, TGF-β signaling can activate the PI3K/AKT pathway in 16HBE cells, [56] and downregulation of TGF-β signaling was found to slow down the activation of PI3K/AKT signaling, thereby reducing EMT and inflammation, in bleomycin-induced fibrosis of mice. [57] PI3K/ AKT inhibitor, in turn, reduced the increased TGF-β1 levels in lung tissues of OVA-sensitized and -challenged mice and reversed TGF-β1-induced EMT and migration of 16HBE cells. [32,58] Consistent with the previously reported inhibitory effects of dioscin on TGF-β and AKT signaling pathways.…”

Section: Effect Of Dioscin On the Tgf-β1-treated 16hbe Cellsmentioning

confidence: 94%

“…[56] The elevated TGF-β1 and p-Smad2/3 took part in fibrosis and inflammation in mice with OVA-induced asthma. [57,58] Additionally, TGF-β1 could enhance chronic airway inflammation in bronchial asthma by recruiting inflammatory cells to the airway. [53] Administration of a TGF-β1 receptor inhibitor significantly elevated IL-6, TNF-α, and IL-17a but decreased IL-10, thus reversing the protective effect of epigallocatechin gallate against airway inflammation in asthmatic mice.…”

Section: Effect Of Dioscin On the Tgf-β1-treated 16hbe Cellsmentioning

confidence: 99%

Dioscin exhibits protective effects on in vivo and in vitro asthma models via suppressing TGF‐β1/Smad2/3 and AKT pathways

Shang

Zhu

Shang

et al. 2022

J Biochem & Molecular Tox

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Dioscin is a natural product that possesses protective effects on multiple chronic injuries, but its effects on asthma are not fully understood. Herein, we evaluated its effects on asthmatic mice established by ovalbumin (OVA) sensitization and challenges and further explored the mechanism. Inflammatory cells in bronchoalveolar lavage fluids (BALFs) were analyzed using Diff‐Quik staining. OVA‐specific immunoglobulin E (IgE)/IgG1 in serum and inflammatory cytokines (interleukin 4[IL‐4], IL‐5, IL‐13, and tumor necrosis factor‐α) in BALFs and lung tissues were measured using Enzyme‐Linked Immunosorbent Assay Kits. Hematoxylin and eosin, periodic acid–Schiff, and immunohistochemistry staining showed histopathological changes in lung tissues. Epithelial–mesenchymal transition (EMT) in human bronchial epithelial (16HBE) cells was assessed by immunofluorescence staining. Hydroxyproline content was used to evaluate collagen deposition. Polymerase chain reaction and Western blot were performed to measure messenger RNA and protein expression. We found that dioscin treatment (particularly at the dose of 80 mg/kg) significantly inhibited pulmonary inflammation in asthmatic mice, as evidenced by the decreased serum OVA‐specific IgE/IgG1 and the reduced inflammatory cells and cytokines in BALFs and lung tissues. Moreover, dioscin effectively ameliorated the goblet cell hyperplasia, mucus hypersecretion, collagen deposition, and smooth muscle hyperplasia in the airways of asthmatic mice. Mechanistically, dioscin restrained the activated TGF‐β1/Smad2/3 and protein kinase B (AKT) signal pathways in lung tissues and potently reversed the TGF‐β1‐induced EMT and phosphorylation of Smad2/3 and AKT in 16HBE cells. Collectively, dioscin displayed protective effects on OVA‐induced asthmatic mice via adjusting TGF‐β1/Smad2/3 and AKT signal pathways, supporting the fact that dioscin could be a candidate for chronic asthma prevention in the future.

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“…Bleomycin was injected in all of the groups, except for the Sham group, in which saline was injected instead. The mice received ATG by intraperitoneal injection for 28 days [ 23 , 24 ], whereas the Sham and PF mice were given saline by intraperitoneal injection.…”

Section: Methodsmentioning

confidence: 99%

Ameliorative Effects of Arctigenin on Pulmonary Fibrosis Induced by Bleomycin via the Antioxidant Activity

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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In this study, we evaluated the in vivo effect of arctigenin (ATG) on bleomycin-induced pulmonary fibrosis in mice and assessed the role of antioxidant activity. Hematoxylin and eosin (H&E) staining, the results of Masson’s trichrome, and Sirius red staining showed that bleomycin induced obvious pathological changes and collagen deposition in the lung tissue of mice, which were effectively inhibited by ATG. Specifically, based on immunohistochemistry and western blot results, ATG inhibited the expression of fibrosis markers, such as collagen, fibronectin, and α-SMA. Moreover, ATG regulated reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) in the lung tissue of pulmonary fibrosis mice and reduced the pressure of oxidative stress. ATG also regulated the TGF-β-induced expression of p-Akt, confirming that ATG can inhibit fibrosis through antioxidant activity modulation.

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Low molecular weight fucoidan attenuating pulmonary fibrosis by relieving inflammatory reaction and progression of epithelial-mesenchymal transition

Cited by 32 publications

References 46 publications

Investigation of Anti-Epithelial-Mesenchymal Transition and Anti-Inflammation effects of Qing Fei Hua Xian Decotion on Pulmonary Fibrosis via Network Pharmacology and Experimental Verification

Investigation of Anti-Epithelial-Mesenchymal Transition and Anti-Inflammation effects of Qing Fei Hua Xian Decotion on Pulmonary Fibrosis via Network Pharmacology and Experimental Verification

Dioscin exhibits protective effects on in vivo and in vitro asthma models via suppressing TGF‐β1/Smad2/3 and AKT pathways

Ameliorative Effects of Arctigenin on Pulmonary Fibrosis Induced by Bleomycin via the Antioxidant Activity

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