Comparative study on the anti-inflammatory and protective effects of different oxygen therapy regimens on lipopolysaccharide-induced acute lung injury in mice

Wu, Xinhe1,#; Shao, Yanan2,#; Chen, Yongmei3; Zhang, Wei3; Dai, Shirong3; Wu, Yajun1; Jiang, Xiaoge2; Song, Xinjian2,*; Shen, Hao2,*.

¹Department of Hyperbaric Oxygen Medicine, Affiliated Nantong Rehabilitation Hospital of Nantong University, Nantong, Jiangsu Province, China²Department of Rehabilitation Medicine, Affiliated Nantong Rehabilitation Hospital of Nantong University, Nantong, Jiangsu Province, China³Department of Pathology, Affiliated Nantong Rehabilitation Hospital of Nantong University, Nantong, Jiangsu Province, China

Abstract

Oxygen therapy after acute lung injury can regulate the inflammatory response and reduce lung tissue injury. However, the optimal exposure pressure, duration, and frequency of oxygen therapy for acute lung injury remain unclear. In the present study, after intraperitoneal injection of lipopolysaccharide in ICR mice, 1.0 atmosphere absolute (ATA) pure oxygen and 2.0 ATA hyperbaric oxygen treatment for 1 hour decreased the levels of proinflammatory factors (interleukin-1beta and interleukin-6) in peripheral blood and lung tissues. However, only 2.0 ATA hyperbaric oxygen increased the mRNA levels of anti-inflammatory factors (interleukin-10 and arginase-1) in lung tissue; 3.0 ATA hyperbaric oxygen treatment had no significant effect. We also observed that at 2.0 ATA, the anti-inflammatory effect of a single exposure to hyperbaric oxygen for 3 hours was greater than that of a single exposure to hyperbaric oxygen for 1 hour. The protective effect of two exposures for 1.5 hours was similar to that of a single exposure for 3 hours. These results suggest that hyperbaric oxygen alleviates lipopolysaccharide-induced acute lung injury by regulating the expression of inflammatory factors in an acute lung injury model and that appropriately increasing the duration and frequency of hyperbaric oxygen exposure has a better tissue-protective effect on lipopolysaccharide-induced acute lung injury. These results could guide the development of more effective oxygen therapy regimens for acute lung injury patients.

摘要：氧疗可调节急性肺损伤的炎症反应，减少肺组织损伤。然而，急性肺损伤的最佳氧气暴露压力、持续时间和治疗频率尚不清楚。因此，实验构建了脂多糖诱导的ICR小鼠急性肺损伤模型。给予1.0 ATA纯氧和2.0 ATA高压氧治疗1h后，见其外周血和肺组织中促炎因子（白细胞介素1β和白细胞介素6）水平明显下降，而只有2.0 ATA高压氧才能增加肺组织中抗炎因子（白细胞介素10和精氨酸酶1）mRNA水平，且3.0ATA高压氧则无明显效果。实验显示了2.0 ATA高压氧单次暴露3h的抗炎作用明显强于单次暴露1h，且两次暴露1.5h的保护作用与单次暴露3h的保护效果接近。表明高压氧可通过调节急性肺损伤模型中炎症因子表达来减轻脂多糖诱导的急性肺损伤。适当增加高压氧暴露的时间和频率对急性肺损伤有更好的保护作用。上述结果可为急性肺损伤患者开发更有效的氧疗方案提供帮助。