Liproxstatin-1 alleviates bleomycin-induced alveolar epithelial cells injury and mice pulmonary fibrosis via attenuating inflammation, reshaping redox equilibrium, and suppressing ROS/p53/α-SMA pathway

Tao, Ningning; Li, Kang; Liu, Jingjing; Fan, Guoqing; Sun, Tieying

doi:10.1016/j.bbrc.2021.02.127

Cited by 23 publications

(13 citation statements)

References 34 publications

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“…It has been found that the long-term efficacy of treatment by simply inhibiting inflammation is unsatisfactory. Subsequently, it has been shown that the occurrence of PF is closely related to the oxidation/antioxidant imbalance caused by the accumulation of ROS [28][29][30]. Compared to healthy individuals, OS biomarkers in the exhaled respiratory condensate of patients with PF contain hydrogen peroxide (H 2 O 2 ) and 8-iso-PGF2 α.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…This circumstantial evidence suggests that macrophage ferroptosis may be an important motivator of fibroblast activation. Furthermore, Li et al and Tao et al found that liproxstatin-1, a ferroptosis inhibitor, functioned to remarkably reduce TGF-β expression and collagen accumulation in the idiopathic pulmonary fibrosis animal model 64,65 . The implications of macrophages in this process needs further exploration.…”

Section: Macrophage Ferroptosis Upon Pm Exposurementioning

confidence: 99%

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2022

j Endocrinol sci

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Occupational exposure to particulate matter (PM) induced pulmonary fibrosis has aroused broad public concern. Pulmonary interstitial fibrosis is a central pathologic process of pneumoconiosis. Meanwhile, ferroptosis is a newly defined iron-dependent programmed cell death (PCD) that features increased intracellular labile iron and lethal accumulation of lipid peroxidation. Ferroptosis has been found to involve particulate-induced cytotoxicity. Recent studies have suggested that ferroptosis is closely associated with the occurrence and progression of pulmonary fibrosis. Here, we present a mini review to summarize the main mechanisms responsible for PM-induced pulmonary fibrosis via inducing macrophage ferroptosis to provide new insights into basic and clinical research of pulmonary fibrosis.

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“…Previous studies have reported that anti-PD-1 immunotherapy could re-invigorate the effector function of CD8 + T cells in TME, which triggered tumor cell ferroptosis by secreting IFN-γ and suppressing the expression of subunits of the glutamate-cystine antiporter system Xc − . 8 9 To confirm whether tumor cell ferroptosis is responsible for the therapeutic effect of anti-PD-1 antibody treatment, we employed liproxstatin-1, a ferroptosis-specific inhibitor in vivo, 33 to treat C57BL/6 mice implanted with B16F10 melanomas and receiving anti-PD-1 antibody treatment (figure 1A). As a result, while anti-PD-1 antibody alone led to the reduction of tumor growth, the systemic administration of liproxstatin-1 could prominently suppress melanoma regression resulting from immunotherapy (figure 1B-D).…”

Section: The Expression Profile Of Mirnas In Ifn-γ-driven Ferroptosis...mentioning

confidence: 99%

Nanoparticle delivery of miR-21-3p sensitizes melanoma to anti-PD-1 immunotherapy by promoting ferroptosis

Guo

Chen

et al. 2022

J Immunother Cancer

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BackgroundAlthough anti-programmed cell death protein 1 (PD-1) immunotherapy is greatly effective in melanoma treatment, low response rate and treatment resistance significantly hinder its efficacy. Tumor cell ferroptosis triggered by interferon (IFN)-γ that is derived from tumor-infiltrating CD8+ T cells greatly contributes to the effect of immunotherapy. However, the molecular mechanism underlying IFN-γ-mediated ferroptosis and related potentially promising therapeutic strategy warrant further clarification. MicroRNAs (miRNAs) participate in ferroptosis execution and can be delivered systemically by multiple carriers, which have manifested obvious therapeutic effects on cancer.MethodsMiRNAs expression profile in IFN-γ-driven ferroptosis was obtained by RNA sequencing. Biochemical assays were used to clarify the role of miR-21-3p in IFN-γ-driven ferroptosis and the underlying mechanism. MiR-21-3p-loaded gold nanoparticles were constructed and systemically applied to analyze the role of miR-21-3p in anti-PD-1 immunotherapy in preclinical transplanted tumor model.ResultsMiRNAs expression profile of melanoma cells in IFN-γ-driven ferroptosis was first obtained. Then, upregulated miR-21-3p was proved to facilitate IFN-γ-mediated ferroptosis by potentiating lipid peroxidation. miR-21-3p increased the ferroptosis sensitivity by directly targeting thioredoxin reductase 1 (TXNRD1) to enhance lipid reactive oxygen species (ROS) generation. Furthermore, miR-21-3p overexpression in tumor synergized with anti-PD-1 antibody by promoting tumor cell ferroptosis. More importantly, miR-21-3p-loaded gold nanoparticles were constructed, and the systemic delivery of them increased the efficacy of anti-PD-1 antibody without prominent side effects in preclinical mice model. Ultimately, ATF3 was found to promote miR-21-3p transcription in IFN-γ-driven ferroptosis.ConclusionsMiR-21–3 p upregulation contributes to IFN-γ-driven ferroptosis and synergizes with anti-PD-1 antibody. Nanoparticle delivery of miR-21–3 p is a promising therapeutic approach to increase immunotherapy efficacy without obvious systemic side effects.

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Liproxstatin-1 alleviates bleomycin-induced alveolar epithelial cells injury and mice pulmonary fibrosis via attenuating inflammation, reshaping redox equilibrium, and suppressing ROS/p53/α-SMA pathway

Cited by 23 publications

References 34 publications

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

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

Untitled

Nanoparticle delivery of miR-21-3p sensitizes melanoma to anti-PD-1 immunotherapy by promoting ferroptosis

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