| BackgroundCurrently, the antibiotic treatment is not satisfactory in the treatment of severe pneumonia on clinical studies,which is still manifested in poor and high mortality rates. At present, studies have shown that severe pneumonia resulting from systemic inflammatory response (SIRS) caused by multiple organ dysfunction syndrome (MODS) are the body defense mechanism caused by the excessive activation of the outcome of its own destruction, not bacteria or toxins, such as a direct injury. The body is at the role of proinflammatory factors that produce pro-inflammatory cytokines,which promote inflammation, stimulate cell defense response,eliminate invading micro-organisms, promote tissue repair; at the same time,the body release anti-inflammatory media, confrontation inflammatory mediators, reduce the generation of inflammatory mediators, so to confine inflammation, control systemic inflammatory response at the appropriate range. If the pro-inflammatory and anti-inflammatory are balance, environmental stability; If any party to gain advantage, there will be SIRS or CARS, and further damage caused by the body itself. Although a simple antibiotic treatment has anti-inflammatory effects, but can not prevent inflammation out of control, domestic and foreign scholars are actively exploring a new mechanism for anti-inflammatory therapy to find new therapeutic approach to improve the cure rate of severe pneumonia.Anti-inflammatory factor and the immune regulation therapy become the new hot spot for treatment of severe pneumonia.The whole test was divided into two partsPart one : Establishment of rat model with severe pneumoniaObjectiveThe purpose of this study is to explore the diagnostic criteria and patho- physiological characteristics of new avenues for the treatment of severe pneumonia in experimental treatment and pharmacodynamics of the treatment delivery platform through the replication model of rats with severe pneumonia, bacterial pneumonia.MethodsFifty-four male SD rats were randomly divided into three groups:control group,severe pneumonia group(model group)and PGE1 group.The model of severe pneumonia were set up in model guoup and PGE1 group by tracheal inoculation of klebsiella after six days.The PGE1 group was injected with Lipo-PGE1 via the tail vein from the sixth day. The control group and model group was injected with the same dose of normal saline from the sixth day. The animals were killed separately in batches on 7th,9th,11th day after inoculation.Dynamic observe animals, peripheral blood and BALF in the white blood cells (WBC), neutrophil (PMN) count, blood gas analysis, lung tissue wet-dry specific gravity and lung tissue pathological changes.Results1,The clinical symptoms of the model group and PGE1 group was significantly worse than the control group.2,The model group and PGE1 group WBC and PMN in eripheral blood and BALF were significantly higher than the control group in the same time at 7th,9th,11th day (P<0.01).The model group and PGE1 group WBC and PMN in eripheral blood and BALF decreased gradually (P<0.05).The PGE1 group WBC and PMN in eripheral blood and BALF were significantly lower than model group at 7th,9th,11th day (P<0.05).The model group and PGE1 group PaO2,PaCO2 and SaO2 have statistically significant difference at 7th,9th day (P<0.01).There was no significant difference between the three groups at 11th day.The model group and PGE1 group PaO2, SaO2 were increased gradually,PaCO2 were decreased gradually at 7th,9th,11th day (P<0.05). The PGE1 treatment can significantly improve the PaO2, SaO2 level, leaving the level of PaCO2 decreased.There was significant difference compared with model group (P<0.05). The ratio of W/D in the model group and PGE1 group have statistically significant difference at 7th,9th day (P<0.01). The ratio of W/D in PGE1 group was significant difference compared with model group (P<0.05) The lung inflammation in model group was significantly increased, The pathological changes in model group were serious compared with the control group.The pathological changes in PGE1 group were significantly reduced compared with the model group.Part two: Experimental study on the effects of Liposomal prostaglandin E1 on the CD4+CD25+ Treg cell of rats with severe pneumoniaObjectiveTo study the effects of liposomal prostaglandin E1 on CD4+CD25+Treg cells in rats with severe pneumonia and discuss its significance.MethodsTake rat peripheral blood and BALF in PGE1 group,the control group and model group on 7th,9th,11th day, percentage of CD4+CD25+regulatory T-cell about CD4+T cells from BALF and blood were measured by flow cytometry methods (FCM).ResultsOn 7th,9th,11th day,In PGE1 group,the ratios of Treg to CD4+ T cells in peripheral blood [(27.32±1.26)%,(24.53±1.32)%,(19.24±2.63)%]were significantly higher than model group [(23.19±2.18)%,(19.80±1.39)%,(15.11±1.73)%] and control group[(5.35±0.77)%,(5.21±0.61)%,(5.46±0.80)%](P<0.05).The ratios of Treg to CD4+ T cells in BALF [(61.88±2.83)%,(55.75±4.19)%,(45.61±2.92)%]were significantly higher than model group[(53.77±4.32)%,(45.69±3.52)%,(39.54±3.99)%] and control group[(20.13±2.47)%,(20.47±2.49)%,(22.11±4.60)%] (P<0.05 or 0.01).Conclusion:1. Intratracheal instillation of Klebsiella pneumoniae can successfully make the rat model of severe pneumonia.2. The ratio of CD4+ CD25+ Treg cell is increased in rat peripheral blood and BALF with severe pneumonia in the model group.Lipo-PGE1 could suppress excessive inflammatory response with severe pneumonia. Probably by increasing the number of CD4+CD25+ Treg cell. |
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