Sevoflurane inhibits ferroptosis: A new mechanism to explain its protective role against lipopolysaccharide-induced acute lung injury

Life Sciences, Journal Year: 2021, Volume and Issue: 275, P. 119391 - 119391

Published: March 24, 2021

Language: Английский

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Clinical Significance of Heme Oxygenase 1 in Tumor Progression

Antioxidants, Journal Year: 2021, Volume and Issue: 10(5), P. 789 - 789

Published: May 17, 2021

Heme oxygenase 1 (HO-1) plays a key role in cell adaptation to stressors through the antioxidant, antiapoptotic, and anti-inflammatory properties of its metabolic products. For these reasons, cancer cells, HO-1 can favor aggressiveness resistance therapies, leading poor prognosis/outcome. Genetic polymorphisms promoter have been associated with an increased risk progression high degree therapy failure. Moreover, evidence from biopsies highlights possible correlation between expression, pathological features, clinical outcome. Indeed, levels tumor specimens often correlate reduced survival rates. Furthermore, modulation has proposed order improve efficacy antitumor therapies. However, contrasting on biology reported. This review focuses as promising biomarker progression; understanding data might guide therapeutic choice outcome patients terms prognosis life quality.

Language: Английский

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Arsenic and antimony co-induced nephrotoxicity via autophagy and pyroptosis through ROS-mediated pathway in vivo and in vitro

Ecotoxicology and Environmental Safety, Journal Year: 2021, Volume and Issue: 221, P. 112442 - 112442

Published: June 21, 2021

Arsenic (As) and antimony (Sb) are commonly accumulated environmental pollutants that often coexist in nature cause serious widespread biological toxicity. To investigate the nephrotoxicity induced by As Sb detail, we explored mechanism which cotreatment autophagy pyroptosis vivo vitro. In this study, mice were treated with 4 mg/kg arsenic trioxide (ATO) or/and 15 trichloride (SbCl3) intragastric intubation for 60 days. TCMK-1 cells ATO (12.5 μM), SbCl3 (25 μM) or a combination of 24 h. The results experiment demonstrated exposure could induce histopathological changes kidneys, increase levels biochemical indicators nephrotoxicity. addition, can co-induce oxidative stress, further activate pyroptosis. an vitro experiment, and/or coexposure increased ROS generation decreased MMP. Moreover, related molecular experiments confirmed coactivated conclusion, our indicated co-exposure via pathway, these two metals might have synergistic effect on

Language: Английский

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Heme oxygenase-1 determines the cell fate of ferroptotic death of alveolar macrophages in COPD

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: May 5, 2023

Background Despite an increasing understanding of chronic obstructive pulmonary disease (COPD) pathogenesis, the mechanisms diverse cell populations in human lung remain unknown. Using single-cell RNA sequencing (scRNA-Seq), we can reveal changes within individual COPD that are important for pathogenesis and characteristics. Methods We performed scRNA-Seq on tissue obtained from donors with non-COPD mild-to-moderate to identify disease-related genes different types. testified findings using qRT−PCR, immunohistochemistry, immunofluorescence Western blotting 25 additional subjects RAW 264.7 macrophages. Targeting ferroptosis inhibitor ferrostatin-1, iron chelator deferoxamine or HO-1 zinc protoporphyrin was administered experimental cigarette smoke mouse model. Results identified two alveolar macrophages (AMs) were dysregulated patients. discovered M2-like AMs modulate susceptibility by disrupting lipid homeostasis both vivo vitro. The discrepancy sensitivity be determined regulated HO-1. In contrast, M1-like showed ability attenuate oxidative stress exert resistance ferroptosis. addition, expression is also involved defects phagocytosis lysosome distortion. This ferroptotic phenotype ameliorated antiferroptotic compounds, chelators inhibitors. During COPD, accumulation peroxidation drives ferroptosis-sensitive AMs, while show characteristics resistance. Ferroptotic M2 lose their anti-inflammatory repair functions but provoke inflammatory responses, resulting consistent inflammation damage presence M1 COPD. Conclusion Appropriate interventions reduce occurrence infections acute onset, delay process.

Language: Английский

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Mitochondrial dysfunction, oxidative stress, ER stress and mitochondria-ER crosstalk alterations in a chemical rat model of Huntington's disease: Potential benefits of bezafibrate

Toxicology Letters, Journal Year: 2023, Volume and Issue: 381, P. 48 - 59

Published: April 26, 2023

Language: Английский

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