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

Life Sciences, Год журнала: 2021, Номер 275, С. 119391 - 119391

Опубликована: Март 24, 2021

Язык: Английский

---

Clinical Significance of Heme Oxygenase 1 in Tumor Progression

Antioxidants, Год журнала: 2021, Номер 10(5), С. 789 - 789

Опубликована: Май 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.

Язык: Английский

---

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

Ecotoxicology and Environmental Safety, Год журнала: 2021, Номер 221, С. 112442 - 112442

Опубликована: Июнь 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

Язык: Английский

---

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

Frontiers in Immunology, Год журнала: 2023, Номер 14

Опубликована: Май 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.

Язык: Английский

---

Inhibition of interleukin-6 trans-signaling improves survival and prevents cognitive impairment in a mouse model of sepsis

International Immunopharmacology, Год журнала: 2023, Номер 119, С. 110169 - 110169

Опубликована: Апрель 12, 2023

Sepsis-associated encephalopathy (SAE) manifests clinically as acute and chronic cognitive impairments, which is associated with increased morbidity mortality. Interleukin-6 (IL-6), a pro-inflammatory cytokine, consistently up-regulated in sepsis. IL-6 initiates proinflammatory effects after binding to soluble receptor (IL-6R) through trans-signalling, requires the transducer gp130. In this study, we investigated whether inhibition of trans-signalling putative therapeutic target for sepsis SAE. Twenty-five patients (12 septic 13 non-septic patients) were recruited study. A significant increase IL-6, IL-1β, IL-10, IL-8 was observed 24 h ICU admission. animal cecal ligation puncture (CLP) used induce male C57BL/6J mice. One hour before or inducing sepsis, mice treated sgp130, selective trans-signaling inhibitor, respectively. Survival rate, cognition, levels inflammatory cytokines, integrity blood-brain barrier (BBB), oxidative stress assessed. addition, immune cells activation transmigration evaluated peripheral blood brains. Sgp130 improved survival rate functions, reduced including TNF-α, MCP-1, plasma hippocampus (hipp), mitigated BBB disruption, ameliorated sepsis-induced stress. also affected monocytes/macrophages lymphocytes Our results indicate that by sgp130 exerts protective against SAE mouse model suggesting potential strategy.

Язык: Английский

---