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ABSTRACT: Acute systemic inflammatory response to severe skin burn injury mediates burn-induced acute lung injury. Ulinastatin is potentially an effective intervention, because it attenuates the systemic inflammatory response induced by endotoxin and improves myocardial function during ischemic shock and reperfusion.
Rats received full-thickness burn wounds to 30% total body surface area followed by delayed resuscitation. The treatment group received 50,000 U/kg of ulinastatin and the burn group was given vehicle only. A sham group was not burned but otherwise was treated identically. After killing, blood and lung samples were harvested for histology and measurement of inflammatory mediators.
Administration of ulinastatin significantly decreased the mRNA and protein levels of tumor necrosis factor-alpha, interleukin-1β, -6, and -8 both locally and systemically in burn-injured rats. The secretion of neutrophil elastase and myeloperoxidase in the lung and the expression of intercellular adhesion molecule-1 on the surface of lung epithelium were inhibited by ulinastatin. Ulinastatin also reduced the increase in pulmonary microvascular permeability. Consistent with these findings, ulinastatin ameliorated the lung edema and pulmonary oxygenation in burn-injured rats.
These results indicate that the inhibitory effects of ulinastatin on inflammatory mediator production, neutrophil activation, and microvascular permeability are associated with the recovery of pulmonary functions in severe burn-induced acute lung injury and suggest that ulinastatin may serve as a potential therapeutic administration in critical burn care.
The Journal of trauma 09/2011; 71(5):1297-304. · 2.48 Impact Factor
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ABSTRACT: To investigate the feasibility of photochemical tissue bonding (PTB) technique in repairing limbal stem cell (LSC) deficiency and the effect on cornea wound healing.
LSCs were isolated from limbus of New Zealand rabbits by tissue block culture method, and then the LSCs of 2nd passage were cultured on de-epithelialized human amniotic membrane (HAM) for 3 weeks to prepare the HAM/LSC grafts. The LSC deficiency models of the left eyes were established by 0.5 mol/L NaOH in 24 New Zealand female rabbits, aged 3-4 months and weighing 1.5-2.0 kg. HAM/LSC grafts were used to repair the cornea wounds by sutures (suture group, n = 12) or by PTB technique (PTB group, n = 12). The gross was observed including the corneal transparency, erythema, and new blood vessel formation after surgery. At 3 and 28 days, the inflammatory cytokine of interleukin 1beta (IL-1beta), IL-6, and tumor necrosis factor alpha (TNF-alpha) were assayed by ELISA method; and the amount of new blood vessels were quantified by immunohistochemistry staining at 28 days.
All animals survived to the end of the experiment. At 3 days, there was no obvious difference in the corneal transparency between 2 groups; at 28 days, the corneal transparency of PTB group was higher than that of suture group, and new blood vessels decreased. HE staining showed that mass inflammatory cells infiltrated between graft and cornea basal layer at 3 days, and no new blood vessel formed. inflammatory cells infiltration significantly decreased at 28 days in PTB group; the amount of new blood vessels was (2.0 +/- 0.8)/HP in PTB group and was (6.3 +/- 1.3)/HP in suture group, showing significant difference (t = 7.966, P = 0.002). At 28 days, the concentrations of inflammatory cytokine of IL-1beta, IL-6, and TNF-alpha in suture group were significantly higher than those in PTB group (P < 0.05); however, no significant differences were observed between 2 groups at 3 days (P > 0.05).
PTB technique can be used to fix HAM/LSC grafts, which can decrease inflammatory cell infiltration and new vessel formation, and improve the outcomes when compared with suture technique.
Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery 09/2011; 25(9):1110-4.
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ABSTRACT: Hydrogen has been reported to selectively quench detrimental reactive oxygen species, particularly hydroxyl radical, and to prevent myocardial or hepatic ischemia/reperfusion injury in multiple models. The aim of this study is to investigate whether hydrogen protects against severe burn-induced acute lung injury in rats. Rats were divided into four groups: sham plus normal saline, burn injury plus normal saline, burn injury plus hydrogen-rich saline, and burn injury plus edaravone. Animals were given full-thickness burn wounds (30% TBSA) using boiling water, except the sham group that was treated with room temperature water. The rats in hydrogen group received 5 ml/kg of hydrogen-rich saline, sham and burn controls obtained the same amount of saline, and the edaravone group was treated with 9 mg/kg of edaravone in saline. Lactated Ringer's solution was given at 6 hours postburn. The lungs were harvested 12 hours postburn for laboratory investigations. Severe burns with delayed resuscitation rapidly caused lung edema and impaired oxygenation in rats. These dysfunctions were ameliorated by administration of hydrogen-rich saline or edaravone. When compared with the burn injury plus normal saline group, hydrogen-rich saline or edaravone group significantly attenuated the pulmonary oxidative products, such as malondialdehyde, carbonyl, and 8-hydroxy-2'-deoxyguanosine. Furthermore, administration of hydrogen-rich saline or edaravone dramatically reduced the pulmonary levels of pulmonary inflammation mediators and myeloperoxidase. Intraperitoneal administration of hydrogen-rich saline improves pulmonary function by reducing oxidative stress and inflammatory response in severe burn-induced acute lung injury.
Journal of burn care & research: official publication of the American Burn Association 03/2011; 32(3):e82-91. · 1.37 Impact Factor
