Home    中文  
 
  • Search
  • lucene Search
  • Citation
  • Fig/Tab
  • Adv Search
Just Accepted  |  Current Issue  |  Archive  |  Featured Articles  |  Most Read  |  Most Download  |  Most Cited

Chinese Journal of Injury Repair and Wound Healing(Electronic Edition) ›› 2025, Vol. 20 ›› Issue (03): 241-247. doi: 10.3877/cma.j.issn.1673-9450.2025.03.009

• Original Articles • Previous Articles     Next Articles

Role of high mobility group protein B1 in liver injury associated with delayed resuscitation following severe burn in rats

Hao Jia1,2, Zhaoxing Liu1, Dawei Li1, Peizhen Li1, Zejin Zhang1, Liwei Liu1, Chuan'an Shen1,()   

  1. 1. Senior Department of Burns and Plastic Surgery,the Fourth Medical Center of PLA General Hospital,Beijing 100048,China
    2. Chinese PLA Medical School,Beijing 100853,China
  • Received:2025-03-05 Online:2025-06-01 Published:2025-06-10
  • Contact: Chuan'an Shen

Abstract:

Objective

To investigate the role and preliminary mechanism of high mobility group protein B1 (HMGB1) in liver injury following delayed resuscitation in rats with severe burns.

Methods

Thirty-two male Sprague-Dawley (SD) rats were randomly divided into sham group, immediate resuscitation group,delayed resuscitation group, and delayed resuscitation+HMGB1-neutralizing antibody group,with 8 rats in each group.A 30% total body surface area (TBSA) full-thickness burn model was established by immersing the rats' dorsum in 98 ℃ water for 12 seconds.Sham group rats were immersed in 37 ℃ water for 12 seconds.The immediate resuscitation group received intraperitoneal injection of lactated Ringer's solution (4 ml·kg-1·1%TBSA-1)immediately after injury, while the delayed resuscitation group and delayed resuscitation+HMGB1-neutralizing antibody group received the same fluid at 6 hours post-injury.The sham group received no resuscitation.Blood and liver tissue samples were collected at 24 hours post-injury.Serum HMGB1 levels were analyzed via enzymelinked immunosorbent assay (ELISA).Serum aspartate aminotransferase (AST) and alanine aminotransferase(ALT) levels were measured using an automated biochemical analyzer.Hematoxylin-eosin (HE) staining was used to assess liver histopathology.Immunohistochemistry was employed to assess the expression of HMGB1 and transforming growth factor-beta (TGF-β) in liver tissues.Western blotting was utilized to quantify the expression of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax).Immunofluorescence staining was utilized for the detection of tumor necrosis factor-alpha (TNF-α) expression.

Results

Compared to the sham group, HMGB1 levels in serum and liver tissues, and serum ALT, AST levels were significantly elevated in the immediate resuscitation group (P<0.05).Compared to the immediate resuscitation group, the delayed resuscitation group showed further increases in HMGB1 and serum ALT, AST levels (P<0.001).Compared to the delayed resuscitation group, HMGB1 levels in serum and liver tissues, and serum ALT, AST levels in the delayed resuscitation+HMGB1-neutralizing antibody group were significantly reduced (P<0.05).Histologically,the sham group exhibited normal hepatocyte morphology and no inflammation.The immediate resuscitation group exhibited mild liver injury, with the basic preservation of the hepatic lobule structure.In this group,liver cells exhibited mild edema or cytoplasmic swelling, and no obvious necrosis or inflammatory response was observed.The delayed resuscitation group showed disordered cell arrangement, diffuse fatty degeneration,and moderate inflammation in liver tissues, while the delayed resuscitation + HMGB1-neutralizing antibody group exhibited reduced fat deposition and mild inflammation.Compared to the delayed resuscitation burn group, the liver tissue injury scores and TNF-α expression were lower in the delayed resuscitation + HMGB1-neutralizing antibody group (P<0.05), with no significant change in TGF-β (P>0.05).Compared with the delayed resuscitation group, the expression of the anti-apoptotic protein Bcl-2 in the liver tissue of the delayed resuscitation + HMGB1-neutralizing antibody group was significantly increased (P=0.009), while the expression of the pro-apoptotic protein Bax was significantly decreased (P=0.021).

Conclusion

HMGB1 mediates liver injury after delayed resuscitation in severe burns, potentially by facilitating apoptosis and inflammatory responses.

Key words: Burns, Delayed resuscitation, Liver injury, High mobility group protein B1

京ICP 备07035254号-3
Copyright © Chinese Journal of Injury Repair and Wound Healing(Electronic Edition), All Rights Reserved.
Tel: 010-58517075 E-mail: zhssyxf@163.com
Powered by Beijing Magtech Co. Ltd