Hyperbaric Oxygen Protects Acute Lung Injury Secondary to Deinagkistrodon Acutus Venom Poisoning by Regulating Th17/Treg Balance.

BACKGROUND

To explore the mechanism of hyperbaric oxygen (HBO) intervention on acute lung injury secondary to Deinagkistrodon acutus snake venom poisoning and provide more toxicological and clinical evidence for Deinagkistrodon acutus venom poisoning.

METHODS

Male Kunming mice (n = 96) were randomly divided into four groups: the control group which was not given any interventional treatments, venom group in which each mouse was injected with Deinagkistrodon acutus venom (1 mg/kg) through the tail vein, antivenom group in which each mouse was injected with anti-Deinagkistrodon acutus venom immediately after the model was successfully established, and HBO+antivenom group in which each mouse was given HBO treatment at 1 h, 5 h, 11 h and 23 h following the injection of antivenom. Lung tissues of mice were obtained and processed for the detection of the lung coefficient, the levels of inflammatory factors such as interleukin (IL)-6, IL-10 and IL-17, and the protein expression of retinoic acid receptor (RAR)-related orphan receptor gamma (RORγt) and forkhead box P3 (FOXP3). Separate lung tissue specimens were acquired for hematoxylin-eosin staining.

RESULTS

Compared with the venom group, HBO+antivenom group exhibited (1) improved survival rate within 24 h; (2) resolution of pulmonary edema, integrity restoration of alveolar structure, and reduced number of infiltrated inflammatory cells; (3) diminished levels of pro-inflammatory factors and increased abundance of anti-inflammatory factors beginning 2 h after envenomation; and (4) balanced expression of RORγt protein and FOXP3 protein at 24 h after envenomation.

CONCLUSION

HBO combined with antivenom can significantly relieve secondary lung injury in mice poisoned with Deinagkistrodon acutus venom by immediately regulating the balance of helper T cell 17 (Th17)/regulatory T cell (Treg) related proteins.