本文選題：促紅細胞生成素　切入點：膿毒癥　出處：《遵義醫(yī)學院》2017年碩士論文

【摘要】：目的:通過建立大鼠膿毒癥急性肺損傷模型,用EPO進行干預,觀察肺組織病理改變及血清中HMGB1、Bcl-2水平變化,探討EPO對膿毒癥急性肺損傷是否具有保護作用。方法:體重為180~200g的健康SD雄性大鼠24只,隨機分成:S組(對照組)、A組(ALI組)、E組(EPO治療組)。建立脂多糖(LPS)二次打擊大鼠ALI模型,即致大鼠雙側(cè)股骨骨折后6h,舌下靜脈注射LPS 5mg/kg進行二次打擊,完成模型制作。E組在LPS二次打擊后立即靜脈注射重組人促紅細胞生成素(rh EPO)1000 IU/kg,A組和S組靜脈注射等量的生理鹽水,8h后獲取肺組織和動脈血。血氣分析檢測Pa O2、Pa CO2、HCO3-、p H值;測定肺組織濕干比值(W/D);ELISA法檢測了血清中HMGB1和Bcl-2水平;右肺上葉固定于4%多聚甲醛中,24h后行HE染色病理學檢查;所得數(shù)據(jù)應用SPSS 17.0軟件進行統(tǒng)計分析。結(jié)果:1)肺組織病理切片結(jié)果:S組大鼠肺泡結(jié)構(gòu)完整,無炎性細胞浸潤;A組大鼠肺泡結(jié)構(gòu)完全破壞,肺泡內(nèi)見炎性細胞浸潤及不等量紅細胞滲出;E組大鼠肺泡結(jié)構(gòu)部分破壞,部分肺泡內(nèi)見灶狀泡沫細胞聚集及少量紅細胞滲出,較A組相比兩者都有不同程度的肺泡損傷及炎性病理改變,但A組肺泡結(jié)構(gòu)破壞更加嚴重,炎性細胞及紅細胞滲出更多。2)肺組織W/D值結(jié)果:肺組織W/D值在A組和E組分別為(6.05±0.64)、(5.33±0.57),與S組(4.48±0.25)相比均明顯升高(P0.01),而A組又高于E組(P0.05)。3)血氣分析結(jié)果:Pa O2在A組和E組分別為(58.4±1.3)mm Hg、(67±3.5)mm Hg,與S組相比(94.8±2.8)mm Hg均明顯降低(P0.01),而A組又明顯低于E組(P0.01);HCO3-、p H值在S組分別為(27.4±1.1)mmol/L、(7.38±0.41),A組分別為(22.4±3.1)mmol/L、(7.25±0.66),E組分別為(24.8±1.7)mmol/L、(7.32±0.42),A組HCO3-、p H值均低于S組(P0.01)和E組(P0.05),而E組HCO3-、p H值又均低于S組(P0.05);S組、A組和E組Pa CO2分別為(41.5±2.7)mm Hg、(40.2±5.8)mm Hg、(43.3±4.2)mm Hg,各組比較差異無統(tǒng)計學意義(P0.05)。4)血清中HMGB1、Bcl-2水平結(jié)果:血清中HMGB1水平在A組和E組分別為(1390.83±178.99)pg/ml、(1208.08±116.45)pg/ml,與S組(359.25±92.89)pg/ml相比均明顯升高(P0.01),而A組又高于E組(P0.05);血清中Bcl-2水平在A組和E組分別為(1.71±0.55)ng/ml)、(2.53±0.38)ng/ml,與S組(4.31±0.86)ng/ml相比均明顯降低(P0.01),而A組又低于E組(P0.05)。結(jié)論:EPO能減輕急性肺損傷大鼠肺組織炎癥反應并下調(diào)血清中HMGB1水平和上調(diào)Bcl-2水平,對膿毒癥急性肺損傷有保護作用。
[Abstract]:Objective: to establish acute lung injury model of sepsis in rats and to observe the pathological changes of lung tissue and the level of HMGB1 Bcl-2 in serum by EPO intervention. To investigate the protective effect of EPO on acute lung injury of sepsis. Methods: Twenty-four healthy male SD rats weighing 180 ~ 200g were randomly divided into two groups: control group (control group A) and Ali group (group E). Lipopolysaccharide (LPS) model of ALI was established in rats. LPS 5mg/kg was injected into sublingual vein 6 hours after bilateral femoral fracture in rats. The pulmonary tissue and arterial blood were obtained in group E after intravenous injection of recombinant human erythropoietin (rhEPO) -rh EPO)1000 IUP (group A) and group S (n = 8 h) immediately after the second strike of LPS. The blood gas analysis was performed to detect the value of Pa O _ 2Pa CO _ 2o _ 2H _ 2O _ 3-HCO3-HCO3-HCO3-HCO3-HCO3-HCO3-HCO3-H in group S and group A (n = 8), respectively. The levels of HMGB1 and Bcl-2 in serum were detected by WR / DX Elisa, and the pathological examination of HE staining was performed in the upper lobe of the right lung after 24 hours fixed in 4% paraformaldehyde. The data were analyzed by SPSS 17.0 software. Results the results of pathological section of lung tissue showed that the alveolar structure of rats in group S was intact, and the alveolar structure of group A was completely destroyed without inflammatory cell infiltration. Inflammatory cell infiltration and erythrocyte exudation were observed in the alveoli of rats in E group, the alveolar structure was partially destroyed, focal foam cells were accumulated in some alveoli and a few red blood cells exudated. Compared with group A, both of them had different degree of alveolar injury and inflammatory pathological changes, but the destruction of alveolar structure in group A was more serious. WR value of lung tissue in group A and E was 6.05 鹵0.64, 5.33 鹵0.57, which was significantly higher than that in group S (4.48 鹵0.25), but in group A was higher than that in group E (P0.05n.3) blood gas analysis showed that WR / D in group A was higher than that in group A and E respectively. Compared with S group, 58.4 鹵1.3)mm hgfg 67 鹵3.5)mm Hg, 94.8 鹵2.8)mm Hg significantly decreased P0.01U, and the HCO3-HCO3-tioph in group A was significantly lower than that in group E (27.4 鹵1.1 mmol / L 7.38 鹵0.41mol / L 7.38 鹵0.41mol / L 7.38 鹵0.41mmol / L), respectively, and the values of HCO3-Ph in group A were 24.8 鹵1.7mmol-L / L 7.32 鹵2.4mmol / L = 7.32 鹵20.4mmol-1, respectively, which were lower than those in group S (P 0.01) and in group E (P < 0.01), respectively, but the values of CO3-pH in group E were 24.8 鹵1.7mmol / L = 7.25 鹵0.66mmol / L = 7.25 鹵0.66kmol / L = 24.8 鹵1.7mmol / L = 7.25 鹵0.66mmol / L = 7.25 鹵0.66mmol / L = 7.25 鹵1.7mmol / L = 7.25 鹵0.66g / h, respectively. It was also lower than that in group S (P 0.05): Pa CO2 of group A and group E were 41.5 鹵2.7)mm 2.7)mm, 40.2 鹵5.8)mm, 43.3 鹵4.2)mm, respectively. There was no significant difference in serum HMGB1Bcl 2. Results: the level of serum HMGB1 in group A and E was 1390.83 鹵178.99pg / ml, 1208.08 鹵116.45pgml / ml, which was significantly higher than that in group S (359.25 鹵92.89)pg/ml, P < 0.05). The serum HMGB1 level in group A and E was 1390.83 鹵178.99p / ml / ml, 1208.08 鹵116.45pgml / ml respectively, which was significantly higher than that in group S (359.25 鹵92.89)pg/ml). The levels of serum Bcl-2 in group A and E were 1.71 鹵0.55 ng / ml and 2.53 鹵0.38 ng / ml, respectively, which were significantly lower than those in group S (4.31 鹵0.86)ng/ml), but lower in group A than in group E (P 0.05). Modulating serum HMGB1 level and up-regulating Bcl-2 level, It has protective effect on acute lung injury of sepsis.
【學位授予單位】：遵義醫(yī)學院
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R459.7

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