Galangin ameliorated pulmonary fibrosis in vivo and in vitro by regulating epithelial-mesenchymal transition

Wang, Liqun; Liu, Hongyao; He, Qiurong; Chai, Guoqiang; Li, Yali; Zhang, Qianyu; Yao, Yuqin; He, Fang; Ye, Tinghong; Yin, Wenya

doi:10.1016/j.bmc.2020.115663

Cited by 19 publications

(17 citation statements)

References 34 publications

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“…P62 and LC3B-II/LC3B-I ratio are key factors in activation of cell autophagy [40,41]. Downregulation of p62 and increase of LC3B-II/LC3B-I could lead to the occurrence of autophagy [42,43]. In addition, Chu et al stated that Tim-1 could trigger autophagy in dengue virus infection [22].…”

Section: Discussionmentioning

confidence: 99%

Tim-1 alleviates lupus nephritis-induced podocyte injury via regulating autophagy

Yu¹,

Zhu²,

Yu³

et al. 2021

cejoi

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Introduction:Lupus nephritis (Ln) is a complication of systemic lupus erythematosus (SLE) which seriously threatens the health of people. Tim-1 is known to be associated with the pathogenesis of SLE. however, the role of Tim-1 in Ln is still unclear.Aim of the study: To explore the expression and the potential regulatory molecular mechanism of Tim-1 in Ln-induced podocyte injury.Material and methods: an in vivo model of Ln was established to detect the expression of Tim-1, inflammatory cytokines and autophagy-related proteins. Podocytes were treated with immunoglobulin g (igg) to establish the Ln in vitro model and then treated with an autophagy inhibitor. RT-qPCR and western blot were performed to investigate the effect of Tim-1 on inflammatory responses as well as autophagy in podocytes. The function of Tim-1 in igg-induced podocytes was detected by CCK-8 and flow cytometry, respectively.Results: Tim-1, L3Bii/L3Bi ratio and inflammatory cytokines were upregulated in Ln mice. Tim-1 notably inhibited igg-induced inflammatory responses in podocytes via reducing tumor necrosis factor α (TnF-α), interleukin (iL)-6 and iL-1β expression, and it could protect podocytes against Ln-induced injury via inducing autophagy. Meanwhile, Tim-1 significantly promoted the proliferation of igg-induced podocytes via inhibiting apoptosis. The autophagy inhibitor reversed the effect of Tim-1 on inflammatory cytokines and autophagy-related proteins in igg-treated podocytes.Conclusions: Tim-1 protects podocytes against Ln-induced injury via mediating autophagy, which might serve as a new target for the treatment of Ln.

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Section: Discussionmentioning

confidence: 99%

Tim-1 alleviates lupus nephritis-induced podocyte injury via regulating autophagy

Yu¹,

Zhu²,

Yu³

et al. 2021

cejoi

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“…It induces Nrf2 signaling and dampens p-IIκBα, NF-κB, EMT transition, TGF-β1, and the p-Smad2/3 pathway [ 193 ]. Galanin is a flavonoid compound that attenuates inflammatory damage and prevents EMT in BLM-induced PF mice [ 198 ].…”

Section: Natural Products Against Pulmonary Fibrosis With Specific Me...mentioning

confidence: 99%

Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis

Hasan

Paul

et al. 2022

Molecules

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Pulmonary fibrosis (PF) is a disease-refractive lung condition with an increased rate of mortality. The potential factors causing PF include viral infections, radiation exposure, and toxic airborne chemicals. Idiopathic PF (IPF) is related to pneumonia affecting the elderly and is characterized by recurring scar formation in the lungs. An impaired wound healing process, defined by the dysregulated aggregation of extracellular matrix components, triggers fibrotic scar formation in the lungs. The potential pathogenesis includes oxidative stress, altered cell signaling, inflammation, etc. Nintedanib and pirfenidone have been approved with a conditional endorsement for the management of IPF. In addition, natural product-based treatment strategies have shown promising results in treating PF. In this study, we reviewed the recently published literature and discussed the potential uses of natural products, classified into three types—isolated active compounds, crude extracts of plants, and traditional medicine, consisting of mixtures of different plant products—in treating PF. These natural products are promising in the treatment of PF via inhibiting inflammation, oxidative stress, and endothelial mesenchymal transition, as well as affecting TGF-β-mediated cell signaling, etc. Based on the current review, we have revealed the signaling mechanisms of PF pathogenesis and the potential opportunities offered by natural product-based medicine in treating PF.

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“…The detection procedures were carried out as previously described. 8 About 30 mg of fresh lung tissue was taken and lysed by collagenase shock for 1.5 h. After washing with PBS, the precipitate was resuspended with 1 mL of PBS. The cell suspension was partitioned into flow cytometry, stained with corresponding antibodies for 30 min at room temperature, and then detected by flow cytometry (ACEA NovoCyte™, ACEA Biosciences).…”

Section: Detection Of Free Radical Scavenging Ability Of Rsjmentioning

confidence: 99%

“…H&E and Masson staining were carried out as previously described. 8 H&E staining was used to observe lung structures, Masson staining was used to observe collagen deposition, and immunohistochemical stain-…”

Section: Detection Of Free Radical Scavenging Ability Of Rsjmentioning

confidence: 99%

“…In the COVID-19 epidemic, natural products derived from traditional Chinese medicines (TCM) showed good preventive effects on pneumonia and even exerted some therapeutic effects on mild disease, 7 and our previous works also found that galangin alleviated bleomycin-induced lung injury. 8 Given these beneficial effects of natural products, researchers are increasingly interested in finding new potential natural products for lung disease therapy.…”

Section: Introductionmentioning

confidence: 99%

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