Redox imbalance is an vital mechanism for COPD. At present, insufficient researches have been conducted on the protective effect of hydrogen sulfide (H₂S) on PM-induced COPD. However, whether H₂S exerts the anti-injury role by blocking ferroptosis and restoring redox equilibrium remain to be investigated. Human lung tissue samples were collected for IHC staining, and the expressions of Nrf2, ferritinophagy- and ferroptosis-related proteins were observed. The WT C57BL/6 and Nrf2 knockout mice models were established with PM(200 μg per mouse). NaHS(Exogenous H₂S) was injected intraperitoneally 30 min in advance. Twenty-nine days later, mice lung tissues were evaluated by HE's and PERLS-DAB's staining. Meanwhile, inflammation and oxidative stress indicators and iron levels were assessed by corresponding ELISA kit. Related protein expressions were detected through Western blot. BEAS-2B cells with or without H₂S were exposed to PM2.5 for 36 h. Cell viability, mitochondrial morphology, inflammatory cytokines, antioxidant factors, iron levels, autophagic flux and the levels of ROS, LIP ROS, MitoROS, MMP, as well as related protein expressions were detected by specific methods, respectively. In addition, V5-Nrf2, Nrf2 siRNA, Nrf2 inhibitor ML385, PPAR-γ inhibitor GW9662, autophagy inhibitor CQ, iron chelator DFO and ferroptosis inhibitor Fer-1 were used to verify the target signaling pathways. We found that the expressions of LIP ROS, ROS, COX2, MDA and other oxidative factors increased, while the antioxidant markers GPX4, GSH and GSH-Px significantly decreased, as well as active iron accumulation in COPD patients, PM-exposured WT and Nrf2-KO mice models and PM2.5-mediated cell models. NaHS pretreatment markedly inhibited PM-induced emphysema and airway inflammation by alleviating ferroptotic changes in vivo and vitro. With the use of V5-Nrf2 overexpression plasmid, Nrf2 siRNA and pathway inhibitors, we found NaHS activates the expressions of Nrf2 and PPAR-γ, and inhibites ferritinophagy makers LC3B, NCOA4 and FTH1 in BEAS-2B cells. Moreover, the anti-ferroptotic effect of NaHS was further verified to be related to the activation of Nrf2 signal in MEF cells. This research suggested that H₂S alleviated PM-induced emphysema and airway inflammation via restoring redox balance and inhibiting ferroptosis through regulating Nrf2-PPAR-ferritinophagy signaling pathway.

Background: While the prevalence and disease burden of bronchiectasis are increasing, data in the world’s largest population are lacking. We aimed to investigate the prevalence and disease burden of bronchiectasis in Chinese adults. Methods: We conducted a population-based study using data between 2013 and 2017 from the national databases of Urban Employee Basic Medical Insurance and Urban Resident Basic Medical Insurance in China. Data from over 380 million patients aged 18 years and older during the study period were analyzed, and a total of 383,926 bronchiectasis patients were identified. Primary outcomes included the age- and sex-specific prevalence of bronchiectasis. Annual visits and hospitalizations, as well as annual costs were also calculated. Results: The prevalence of bronchiectasis in Chinese adults increased 2.31-fold, from 75.48 (62.26, 88.69) per 100,000 in 2013 to 174.45 (137.02, 211.88) per 100,000 in 2017. The increase was more remarkable for patients aged over 50 years in both genders. The per-capita total cost and hospitalization cost of patients with bronchiectasis increased 2.18-fold and 1.83-fold from 2013 to 2017, respectively, mostly driven by non-bronchiectasis costs. The average annual hospitalization ranged from 1.20 to 1.24 times during the 5 years. Conclusion: The prevalence and disease burden of bronchiectasis in Chinese urban adults ≥ 18 years had increased significantly between 2013 and 2017.