Early Hyperbaric Oxygen Therapy Promotes Recovery of Blunt Liver Injury in Rats via Inhibiting Inflammatory Response and Oxidative Stress

Abstract

Purpose: Blunt Liver Injury (BLI) is a common form of blunt abdominal trauma, with most cases managed non-surgically in current clinical practice. However, the absence of targeted treatments addressing the pathological changes associated with liver injury can result in prolonged recovery and potential long-term complications. Hyperbaric oxygen therapy (HBOT), known for its anti-inflammatory and antioxidant effects, has shown therapeutic potential in various diseases. This prospective randomized controlled experimental animal trial aimed to evaluate the effect of HBOT on BLI in a rat model. Methods: We established a BLI rat model by employing a free-fall weight method. Following injury, one group received no intervention, while the other was treated with HBOT (2.5 ATA, 60 minutes per session, once daily). Liver tissue and serum samples were collected at multiple time points for histological evaluation (HE staining), apoptosis detection (TUNEL staining), proliferation assessment (Ki67 immunohistochemical staining), and measurements of liver transaminase (ALT, AST), inflammatory markers (IL-1β, IL-6, TNF-α), and oxidative stress indicators (SOD, MDA, GSH). Results: The results indicated that HBOT significantly reduced liver transaminase elevation, pathological damage, and hepatocyte apoptosis while promoting hepatocyte proliferation and accelerating liver function recovery. Mechanistically, HBOT alleviated oxidative stress and inflammatory response, highlighting its therapeutic potential. Conclusion: These findings provide further evidence supporting the application of HBOT in the clinical management of BLI. This study helps advance the clinical approach to BLI by shifting the focus from symptom management to mechanism-based treatment.

Keywords: blunt liver injury; hyperbaric oxygen therapy; inflammatory response; oxidative stress.

Figure 1

HBOT alleviated BLI in rats. (A) Experimental flowchart. (B) Gross morphology of the liver. (C) Levels of AST, ALT in plasma. Data were expressed as mean ± SEM. Independent samples t-Test was performed between two groups at each time point; ^*p<0.05, ^**p<0.01, ^***p<0.001 and ^****p<0.001. n=6.

Figure 2

HBOT alleviated BLI-induced pathological changes and hepatocyte apoptosis in rats. (A) HE staining of the liver. (B) Tunel staining of the liver. Scale bar = 20μm. n=3.

Figure 3

HBOT promotes cell proliferation following BLI. (A) Ki67 IHC staining of the liver. Scale bar = 20μm. (B) The Proportion of Ki67-Positive Cells. Data were expressed as mean ± SEM. Independent samples t-Test was performed between two groups at each time point; ^*p<0.05, ^**p<0.01, ^***p<0.001 and ^****p<0.001. n=3.

Figure 4

HBOT alleviated BLI-induced oxidative stress in rats. Concentration of SOD (A), MDA (B), GSH (C) in the liver. Data were expressed as mean ± SEM. Independent samples t-Test was performed between two groups at each time point; ^*p<0.05, ^**p<0.01, ^***p<0.001 and ^****p<0.001. n=6.

Figure 5

HBOT alleviated BLI-induced inflammatory response in rats. Concentration of IL-1β (A), IL-6 (B), TNF-α (C) in the liver. Concentration of IL-1β (D), IL-6 (E), TNF-α (F) in serum. Data were expressed as mean ± SEM. Independent samples t-Test was performed between two groups at each time point; ^*p<0.05, ^**p<0.01, ^***p<0.001 and ^****p<0.001. n=6.