Effect Of Hydrogen-rich Saline On Rat Smoke Inhalation Injury In Different Time Phase

ObjectiveInhalation injury is the respiratory tract and lung parenchyma injury that caused by smoke and (or) thermal, is one of the main causes of death in patients with burns. Its mechanism is closely related with systemic inflammatory response caused by injury. In this study, the design is based on the mature model of rat smoke inhalation injury. After the smoke inhalation injury, the rats were injected hydrogen-rich saline by intraperitoneal in different time. By detecting the rats’serum levels of TNF-a, lung tissue concentration of MDA, SOD, and NF-κBp65, apoptosis, changes of pathological and subcellular structure, to measure the protective effect of hydrogen-rich saline on lung injury, explore the optimal dosing time points, and provide the new idea for clinical treatment.MethodsSeventy-two male Sprague-Dawlay rats were randomly divided into normal control group (n=18), injury control group (n=18), saline group (NS group n=18) and hydrogen-rich saline group (HS group n=18). Injury control group, NS and HS group was used to establish the smoke inhalation injury model. The normal control group has received nothing. After the smoke inhalation injury, six rats extracted from NS and HS group respectively was given saline and hydrogen-rich saline (5mL/kg) by intraperitoneal injection at2h,6h and12h, injury control group received no treatment. After24hours of injured, all serums and lung tissue homogenate were prepared for detection of tumor necrosis factor-a (TNF-a), MDA content and SOD activity. The NF-κBp65of lung tissue was detected by immunohistochemistry. The apoptosis of all lung tissues were also tested with technology of Tunel, and were calculated for apoptotic index (AI). The pathological changes in lung tissue were examined under an optical microscope and the subcellular structure changes also examined under a transmission electron microscope.Results1. The level of TNF-α:the injury control group, NS and HS group were significantly increased compared with normal control group; NS group had the same change with the injury control group (P>0.05); HS group was significantly decreased compared with NS group in each corresponding time phase (P<0.05); in HS group:HS2h<HS6h<HS12h(P<0.05).2. The content of MDA:the injury control group, NS and HS group were significantly increased compared with normal control group; NS group had the same change with the injury control group (P>0.05); HS group was significantly decreased compared with NS group in each corresponding time phase (P<0.05); in HS group:HS2h<HS6h<HS12h(P<0.05).3. The activity of SOD:the injury control group, NS and HS group were significantly decreased compared with normal control group; NS group had the same change with the injury control group (P>0.05); HS group was significantly increased compared with NS group in each corresponding time phase (P<0.05); in HS group:HS2h>HS6h> HS12h(P<0.05).4. The expression rate of NF-κBp65:the injury control group, NS and HS group were significantly increased compared with normal control group; NS group had the same change with the injury control group (P>0.05); HS group was significantly decreased compared with NS group in each corresponding time phase (P<0.05); in HS group:HS2h<HS6h<HS12h (P<0.05).5. The AI:the injury control group, NS and HS group were significantly increased compared with normal control group; NS group had the same change with the injury control group (P>0.05); HS group was significantly decreased compared with NS group in each corresponding time phase (P<0.05); in HS group: HS2h<HS6h<HS12h (P<0.05).6. Under light microscope, in normal control group, the rats alveolar structural integrity and the wall smooth; In injury control group, NS and HS group, the rats alveolar wall thickening and interstitial lung inflammatory cell infiltration; NS group had the same change with the injury control group; In inflammation, inflammatory cell Infiltration and tissue edema, HS group was significantly reduced compared with NS group in each corresponding time phase. In HS group,2h group pathological changes were better than6h,12h group, and6h group was slightly better than12h group. Conclusions1. After inhalation injury, hydrogen-rich saline could play a protective effect on lung tissue by reduced the level of TNF-a, the expression rate of NF-κBp65, the content of MDA, and increased SOD activity, and inhibit tissue apoptosis.2. Hydrogen-rich saline has a better protective effect on the earlier time phase of acute lung injury induced by smoke inhalation injury.3. After inhalation injury, hydrogen play the protective effect on the organization.