ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Obstetric and Pediatric Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1621190
Heliox Preconditioning Exerts Pulmonary Protection Efects on Neonatal Acute Respiratory Distress Syndrome by Inhibiting Oxidative Stress and Apoptosis
Provisionally accepted- 1Children’s Hospital of Chongqing Medical University, Chongqing, China
- 2Department of Pediatrics, First Affiliated Hospital of Army Medical University, Chongqing, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Objective: This study aimed to investigate whether heliox preconditioning (HePC) alleviates neonatal acute respiratory distress syndrome (ARDS) by inhibiting oxidative stress and apoptosis, and to explore its potential mechanism.Methods: Blood samples and bronchoalveolar lavage fluid (BALF) were collected from rat pups were randomly divided into control group, sham group, ARDS group, ARDS+CaMKII -group, ARDS+CaMKII + group, and ARDS+HePC group. We also investigated the role of CaMKII by manipulating its expression in vitro. Inflammatory markers, oxidative stress,apoptosis and activation of signaling pathways were assessed using histological staining, ELISA, Western blotting, qRT-PCR , Ca 2+ , immunofluorescence staining, and flow cytometry. Results: In vivo, HePC significantly reduced the expression of CaMKII, inhibited the activation of CaMKII/RyR2, ameliorated the LPS-induced lung histopathological changes in rat pups, reduced lung wet/dry ratios, ROS and MDA levels, and pro-inflammatory cytokine levels, and significantly increased the expression of antioxidant proteins (Nrf2, HO-1 and SOD) and reduced LPS-induced apoptosis. In vitro, overexpression of CaMKII increases oxidative stress and activates RyR2, leading to cytoplasmic Ca 2+ overload and increased apoptosis. HePC can reverse the above reactions by inhibiting the expression of CaMKII. Conclusions: HePC may attenuate oxidative stress through CaMKII and alleviate cytoplasmic Ca 2+ overload by regulating CaMKII/RyR2, which inhibits apoptosis, exerting lung protection against ARDS.
Keywords: heliox preconditioning, neonatal acute respiratory distress syndrome, CaMK-II, anti-oxidative stress, anti-apoptosis
Received: 30 Apr 2025; Accepted: 29 Jul 2025.
Copyright: © 2025 Ma, Shen and Shi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yuan Shi, Children’s Hospital of Chongqing Medical University, Chongqing, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.