title: Protective effects of ulinastatin on pulmonary damage in rats following scald injury.
abstract: Organ protection is desirable in severe burn/scald injuries, and damage mechanisms and thus effective therapies following scald injury have not been fully elucidated. Our aim was to examine the beneficial effects of ulinastatin on pulmonary damage associated with scald injury. Lewis rats were subjected to 30% total body surface area (TBSA) scald injury and were randomly divided into a burn control (S group) and an ulinastatin-treated group (U group). Lung malondialdehyde (MDA) and superoxide dismutase (SOD) levels were determined, and the lungs were examined histologically with immunohistochemistry (IHC) as well for the major histocompatibility complex (MHC) class I chain-related antigen A (MICA) and Bcl-2 at 24, 48 and 72 h after the injury. The expression of spleen human leucocyte antigen-DR (HLA-DR) was detected by immunohistochemistry analysis. Selectins and adhesion molecules in lungs and serum were also detected. The lung injury degree was represented as wet/dry (W/D) values and alveolar thickness. Ulinastatin decreased MDA levels and ameliorated the down-regulation of SOD activity. MICA was up-regulated after the scald, and this up-regulation was greatly diminished by ulinastatin. Bcl-2 was up-regulated after the scald, especially in the U group. The spleen HLA-DR expression demonstrated the immunoregulatory effects of ulinastatin, which effectively protected the pulmonary tissues from scald-induced injury. Our results demonstrated that pulmonary damage was associated with autoimmunity and oxidant attack after severe scald. Ulinastatin exhibits significant protective effects on these effects.
authors.affiliation: Emergency Department and Surgical Intensive Care Unit, Shanghai 10th People's Hospital, Tongji University School of Medicine, Shanghai, China. chengjingao2003@yahoo.com.cn
authors.forename: Chengjin
authors.initials: C
authors.lastname: Gao
authors.forename: Yuhao
authors.initials: Y
authors.lastname: Liu
authors.forename: Lijie
authors.initials: L
authors.lastname: Ma
authors.forename: Sheng
authors.initials: S
authors.lastname: Wang
mesh_terms: D000818:Animals; D002056:Burns / Q000150:complications* / Q000378:metabolism; D015536:Down-Regulation; D006023:Glycoproteins / Q000627:therapeutic use*; D006684:HLA-DR Antigens / Q000187:drug effects / Q000378:metabolism; D015395:Histocompatibility Antigens Class I / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D055370:Lung Injury / Q000150:complications / Q000378:metabolism / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D019087:Selectins / Q000187:drug effects / Q000378:metabolism; D013482:Superoxide Dismutase / Q000187:drug effects / Q000378:metabolism; D014361:Trypsin Inhibitors / Q000627:therapeutic use*; D015854:Up-Regulation; D019010:Vascular Cell Adhesion Molecule-1 / Q000187:drug effects / Q000378:metabolism
chemical_list: D006023:Glycoproteins; D006684:HLA-DR Antigens; D015395:Histocompatibility Antigens Class I; C099187:MHC class I-related chain A; D019253:Proto-Oncogene Proteins c-bcl-2; D019087:Selectins; D014361:Trypsin Inhibitors; D019010:Vascular Cell Adhesion Molecule-1; D008315:Malondialdehyde; D013482:Superoxide Dismutase; C028665:urinastatin