Topiroxostat ameliorates oxidative stress and inflammation in sepsis-induced lung injury

Abstract

<jats:title>Abstract</jats:title><jats:p>Sepsis-induced lung injury was the most common cause of death in patients. Topiroxostat, a novel xanthine oxidoreductase inhibitors, possessed obvious organ protectives effects. Xanthine oxidase played a vital role in acute lung injury. The study aimed to investigate the roles of Topiroxostat in sepsis-induced lung injury. The sepsis rats were established using cecum ligation and perforation. The lung damage induced by sepsis was evaluated by Hematoxylin and Eosin staining and lung tissue wet to dry ratio. The oxidative stress was detected by measurement of reactive oxygen species, malondialdehyde, myeloperoxidase and superoxide dismutase (SOD). The pro-inflammatory mediators, tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and monocyte chemotactic protein 1, were measured by Enzyme-Linked Immunosorbent Assay. The cell apoptosis in lung was detected by TUNNEL staining and western blot analysis of apoptosis-related proteins including pro-apoptosis proteins, Bax, cleaved caspase9, cleaved caspase3 and anti-apoptosis protein Bcl2. The results showed that Topiroxostat significantly reduced lung damage, along with decreased oxidative stress, inflammation response and apoptosis in sepsis rats. Topiroxostat exerted markedly protective effects in sepsis-induced lung injury and could be an antioxidant in treating sepsis-induced lung injury.</jats:p>

Endogenous Sulfur Dioxide Improves the Survival Rate of Sepsis by Improving the Oxidative Stress Response during Lung Injury

“…This study also found that the oxidation system indicators of the oxidative stress response in sepsis group including H 2 O 2 , MDA, NO level, and MPO activity increased compared with the control group. This result is the same as the results of Rasooli et al [21], antioxidant system indicators including SOD activity and GSH-px level are reduced, and the above results are consistent with previous 7 Oxidative Medicine and Cellular Longevity research results [22][23][24], once again confirming that oxidation and antioxidant imbalance take part in the pathogenesis of septic lung injury. Other studies have also confirmed that sulfur dioxide could regulate the oxidative stress response [25,26].…”

Tumor Suppressor miR-613 Alleviates Non-Small Cell Lung Cancer Cell via Repressing M2 Macrophage Polarization

“…By contraries, fow cytometry analysis expounded that the miR-613 overexpression enhanced the H1650 cell apoptosis (Figure 2(c)). Bax, Bcl-2, and cleaved-caspase-3 were apoptosis-related proteins [26]. As displayed in Figure 2(d), Bax and cleaved-caspase-3 were elevated after miR-613 mimic transfection, while the Bcl-2 was decreased.…”

6-Gingerol attenuates sepsis-induced acute lung injury by suppressing NLRP3 inflammasome through Nrf2 activation

“…Oxidative stress also plays a key role in ALI development [38,55]. ROS attacks different organs, leading to lipid peroxidation, a mutation in the DNA molecule, and protein inactivation [56].…”