title: Effects of Ligustrazine on pulmonary damage in rats following scald injury.
abstract: Organ protection is a routine therapy in severe burn/scald injuries, and damage mechanisms following early scald injury was not been fully elucidated. Our aim was to verify the beneficial effects of Ligustrazine 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 Ligustrazine-treated group (L group). Lung malondialdehyde (MDA) and superoxide dismutase (SOD) levels were determined and the lungs were examined histologically with immunohistochemistry (IHC) as well for the MHC class I chain-related antigen A (MICA) and Bcl-2 at 24, 48 and 72h after the injury. The expression of spleen HLA-DR was detected by immunohistochemistry analysis. Selectins and adhesion molecules in lungs and serum as well as pulmonary interleukins were also detected. The lung injury degree was represented as wet/dry (W/D) values and alveolar thickness. Ligustrazine 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 Ligustrazine. Bcl-2 was up-regulated after the scald, especially in the L group. The spleen HLA-DR expression demonstrated the immunoregulatory effects of Ligustrazine, which effectively protected pulmonary tissues from scald-induced injury. Our results demonstrated that pulmonay damage associated with autoimmunity and oxidant attack occurred after severe scald. Ligustrazine 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, 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: Xiangyu
authors.initials: X
authors.lastname: Zhang
authors.forename: Sheng
authors.initials: S
authors.lastname: Wang
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000209:etiology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D002056:Burns / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D015395:Histocompatibility Antigens Class I / Q000378:metabolism; D007150:Immunohistochemistry; D008168:Lung / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011719:Pyrazines / Q000627:therapeutic use*; D011897:Random Allocation; D051381:Rats; D011917:Rats, Inbred Lew; D013154:Spleen / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D014665:Vasodilator Agents / Q000627:therapeutic use*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015395:Histocompatibility Antigens Class I; C099187:MHC class I-related chain A; D019253:Proto-Oncogene Proteins c-bcl-2; D011719:Pyrazines; D014665:Vasodilator Agents; D008315:Malondialdehyde; D013482:Superoxide Dismutase; C017953:tetramethylpyrazine