2024 · Mu — Hydrogen regulated pyroptosis through NLRP3-GSDMD pathway to improve airway mucosal oxidative stress injury induced by endotracheal tube cuff compression.
Super-Abstract
Endotracheal tube cuffs compress airway tissue during anaesthesia, triggering oxidative stress and a form of inflammatory cell death (pyroptosis) — and hydrogen inhalation or hydrogen-rich saline in the cuff significantly reduced this damage. In patients under general anaesthesia, filling the cuff with hydrogen-rich saline cut postoperative sore throat rates markedly. (Free Radical Biology and Medicine, 2024.)
Commentary
This study bridges laboratory mechanism and clinical application unusually well for this research area. The mechanistic part — knockdown and overexpression of NLRP3 in airway epithelial cells — cleanly demonstrates that H₂ acts by inhibiting the NLRP3-GSDMD pyroptosis pathway, reducing reactive oxygen species and protecting against ischaemia-reperfusion injury in compressed mucosa. The clinical translation is pragmatic: simply replacing air in the endotracheal cuff with hydrogen-rich saline (a zero-cost modification in principle) produced a measurable reduction in postoperative sore throat, which affects a large proportion of intubated patients. This is one of the more clinically actionable H₂ papers because it does not require any new equipment or oral supplementation.
Key quotes
- „Inhalation of hydrogen effectively reduced the levels of reactive oxygen species, significantly ameliorating changes in epithelial cell pyroptosis, and this protective effect is linked to the inhibition of the NLRP3-GSDMD pathway.“ — the mechanistic finding: H₂ acts via NLRP3-GSDMD pyroptosis inhibition
- „using hydrogen-rich saline to inflate the ETT cuff in patients under general anesthesia significantly reduced postoperative sore throat.“ — the clinical translation: cuff saline with H₂ reduces a common postoperative complication
- „hydrogen effectively enhances tolerance of airway mucosa to oxidative stress injuries, offering a potential preventive and therapeutic strategy for protecting the airway mucosa in patients undergoing endotracheal intubation.“ — the summary statement on H₂'s protective role in airway mucosa
Our assessment
One of the more clinically concrete H₂ papers: laboratory mechanisms are tied to a directly measurable, patient-relevant outcome (postoperative sore throat). The NLRP3-GSDMD pathway is a well-established inflammation cascade, and H₂'s inhibition of it is mechanistically coherent. Limitations: the clinical arm's sample size is not reported in the abstract; the postoperative sore throat endpoint, while patient-relevant, is soft (subjective); the mechanism was established in cellular models first, with clinical data following — the sequence is logical but the clinical sample needs scrutiny. The cuff-saline modification would require formal clinical trial data before adoption in anaesthesia practice.
Study design
- Type: combined mechanistic study (in vitro cellular + in vivo) and clinical observation · H₂ delivery: inhalation (mechanistic arm) + hydrogen-rich saline in ETT cuff (clinical arm)
- Mechanism: H₂ reduces ROS → inhibits NLRP3-GSDMD pyroptosis pathway → protects airway epithelial cells from compression-induced ischaemia-reperfusion injury
- Clinical result: hydrogen-rich saline ETT cuff inflation significantly reduced postoperative sore throat in general anaesthesia patients; no adverse effects reported
Abstract
The cuff of endotracheal tube (ETT) is an indispensable device for establishing an artificial airway, yet cuff-induced compression often causes damage to the airway mucosa. The mechanism of this damage involves mucosal compression ischemia and the oxidative stress injury following reperfusion. Currently, there is a lack of effective strategies to protect the mucosa. Hydrogen, as a natural antioxidant, has demonstrated significant potential in the prevention and treatment of oxidative stress injuries. This study aimed to determine the protective effects of hydrogen on compressed airway mucosa. We found that the damage to the airway mucosa caused by ETT cuff compression was associated with oxidative stress-induced pyroptosis of airway epithelial cells. Inhalation of hydrogen effectively reduced the levels of reactive oxygen species, significantly ameliorating changes in epithelial cell pyroptosis, and this protective effect is linked to the inhibition of the NLRP3-GSDMD pathway. Further cellular studies, involving knockdown and overexpression of NLRP3, clarified that hydrogen exerts its protective effects on the airway mucosa by inhibiting epithelial cell pyroptosis. Additionally, we observed that using hydrogen-rich saline to inflate the ETT cuff in patients under general anesthesia significantly reduced postoperative sore throat. This study confirms that hydrogen effectively enhances tolerance of airway mucosa to oxidative stress injuries, offering a potential preventive and therapeutic strategy for protecting the airway mucosa in patients undergoing endotracheal intubation.
Source & links
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