Emodin inhibiting epithelial‐mesenchymal transition in pulmonary fibrosis through the <scp>c‐MYC</scp>/<scp>miR</scp>‐182‐5p/<scp>ZEB2</scp> axis

Yang, Jia; Jiang, Gangdan; Ni, Kaiwen; Fan, Liming; Wang, Tong; Junchao, Yang

doi:10.1002/ptr.7680

Cited by 4 publications

(2 citation statements)

References 40 publications

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“…Emodin is a naturally produced anthraquinone, mainly isolated from Rheum palmatum and Polygonum cuspidatum [ 109 ]. There have been some studies about the regulation of EMT by emodin, mainly focused on two aspects: anti-cancer and anti-fibrosis.…”

Section: Phytochemicals With the Effects Of Interfering Emtmentioning

confidence: 99%

Anti-Cancer Potential of Phytochemicals: The Regulation of the Epithelial-Mesenchymal Transition

Liu

Ren

2023

Molecules

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A biological process called epithelial-mesenchymal transition (EMT) allows epithelial cells to change into mesenchymal cells and acquire some cancer stem cell properties. EMT contributes significantly to the metastasis, invasion, and development of treatment resistance in cancer cells. Current research has demonstrated that phytochemicals are emerging as a potential source of safe and efficient anti-cancer medications. Phytochemicals could disrupt signaling pathways related to malignant cell metastasis and drug resistance by suppressing or reversing the EMT process. In this review, we briefly describe the pathophysiological properties and the molecular mechanisms of EMT in the progression of cancers, then summarize phytochemicals with diverse structures that could block the EMT process in different types of cancer. Hopefully, these will provide some guidance for future research on phytochemicals targeting EMT.

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Section: Phytochemicals With the Effects Of Interfering Emtmentioning

confidence: 99%

Anti-Cancer Potential of Phytochemicals: The Regulation of the Epithelial-Mesenchymal Transition

Liu

Ren

2023

Molecules

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“…The features of pulmonary fibrosis include excessive extracellular matrix deposition, fibroblast foci accumulation, and chronic inflammation (Hewlett et al, 2018). Evidence suggests that epithelial-mesenchymal transition (EMT) process is a contributing factor to the development of pulmonary fibrosis (Yang et al, 2023;Junjie et al, 2023;Ding et al, 2023). EMT refers to a process that epithelial cells transit into cells of mesenchymal phenotype, such as fibroblasts (Kyung et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Ephedrine alleviates bleomycin-induced pulmonary fibrosis by inhibiting epithelial-mesenchymal transition and restraining NF-κB signaling

Tian,

Wang,

2023

J. Toxicol. Sci.

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Pulmonary fibrosis is a lethal and progressive pulmonary disorder in human beings. Ephedrine is a compound isolated from Ephedra and plays a regulatory role in inflammatory response. This study focused on the anti-pulmonary fibrosis effect of ephedrine and its potential molecular mechanism. After a mouse model of pulmonary fibrosis was established through bleomycin (BLM) induction, the survival percentage, body weight, and pulmonary index were measured. Hematoxylin-eosin staining and Masson's trichrome staining for lung tissues were performed to observe the pathological alterations. The viability of lung epithelial BEAS-2B cells, intracellular production of reactive oxygen species, and the levels of pro-inflammatory cytokines were examined by cell counting kit-8 assays, 2ʹ,7ʹdichlorofluorescein diacetate (DCF-DA) staining, and enzyme-linked immunosorbent assay, respectively. Immunofluorescence staining was performed to determine E-cadherin and vimentin expression after BLM or ephedrine treatment. The mRNA and protein levels of cytokeratin-8, E-cadherin, α-SMA, and vimentin were subjected to quantitative polymerase chain reaction and immunoblotting. Experimental results revealed that ephedrine treatment rescued the repressive impact of BLM on BEAS-2B cell viability, and ephedrine inhibited BLM-induced overproduction of reactive oxygen species and inflammatory response in BEAS-2B cells. Additionally, ephedrine suppressed epithelial-mesenchymal transition (EMT) process stimulated by BLM treatment, as demonstrated by the reduced α-SMA and vimentin levels together with the increased cytokeratin-8 and E-cadherin levels in BLM + Ephedrine group. In addition, ephedrine inhibited NF-κB and activated Nrf-2 signaling in BLM-treated BEAS-2B cells. Moreover, ephedrine ameliorated pulmonary fibrosis in BLM-induced mice and improved the survival of model mice. In conclusion, ephedrine attenuates BLM-evoked pulmonary fibrosis by repressing EMT process via blocking NF-κB signaling and activating Nrf-2 signaling, suggesting that ephedrine might become a potential antipulmonary fibrosis agent in the future.

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Forsythiaside A ameliorates bleomycin‐induced pulmonary fibrosis by inhibiting oxidative stress and apoptosis

Yang,

Zhang,

Wang

et al. 2024

Immunity Inflam & Disease

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BackgroundPulmonary fibrosis (PF) is a common clinically critical disease characterized by high morbidity and high mortality. Forsythiaside A (FA) is a phenylethanol glycoside component in Forsythia suspensa, which has anti‐inflammatory, antioxidant, and antiviral activities. However, the effects of FA on bleomycin (BLM)‐induced PF are unclear.PurposeThe present study explored the role of FA in the amelioration of oxidative stress and apoptosis in BLM‐induced PF as well as the possible underlying mechanisms, in vivo and in vitro.MethodsNetwork pharmacology was used to collect the effects of FA on BLM‐induced PF. Subsequently, further observation of the effects of FA on mice with PF by pulmonary pathological changes, transmission electron microscopy, real‐time polymerase chain reaction, Western blot analysis, immunofluorescence, and immunohistochemistry. An in vitro model was constructed by inducing A549 with transforming growth factor beta‐1 (TGF‐β1) to observe the effect of FA on epithelial cell apoptosis.ResultsNetwork pharmacology predicted signaling pathways such as IL‐17 signaling pathway and Relaxin signaling pathway. The results of in vivo studies showed that FA ameliorated BLM‐induced PF through inhibition of fibrosis, modulation of apoptosis, and oxidative stress. In addition, FA promoted TGF‐β1‐induced apoptosis in A549 cells.ConclusionsThe results of our study suggested that FA could protect mice against BLM‐induced PF by regulating oxidative stress and apoptosis as well as the Epithelial mesenchymal transition pathway.

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Emodin inhibiting epithelial‐mesenchymal transition in pulmonary fibrosis through the c‐MYC/miR‐182‐5p/ZEB2 axis

Cited by 4 publications

References 40 publications

Anti-Cancer Potential of Phytochemicals: The Regulation of the Epithelial-Mesenchymal Transition

Anti-Cancer Potential of Phytochemicals: The Regulation of the Epithelial-Mesenchymal Transition

Ephedrine alleviates bleomycin-induced pulmonary fibrosis by inhibiting epithelial-mesenchymal transition and restraining NF-κB signaling

Forsythiaside A ameliorates bleomycin‐induced pulmonary fibrosis by inhibiting oxidative stress and apoptosis

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