ATP－MgCl_2对烫伤大鼠肠粘膜保护作用的实验观察

为研究ＡＴＰ－ＭｇＣｌ２对创伤应激动物肠粘膜的保护作用，采用３０％ＴＢＳＡⅢ度烫伤大鼠模型，观察了腹腔注射ＡＴＰ－ＭｇＣｌ２复合液对回肠粘膜丙二醛（ＭＤＡ）含量及回肠组织形态学改变的影响。结果显示：烫伤后６～２４小时，ＭＤＡ含量明显升高，并伴有形态学病理改变。经ＡＴＰ－ＭｇＣｌ２注射治疗的大鼠伤后２４小时内ＭＤＡ含量维持于正常对照水平，且回肠粘膜病理改变减轻。提示：ＡＴＰ－ＭｇＣｌ２能够保护烫伤大鼠肠粘膜，其作用机理可能与降低肠粘膜的脂质过氧化反应有关。     

ATP—MgCl2对烫伤大鼠肠粘膜保护作用的实验观察

为研究ＡＴＰ－ＭｇＣｌ２对创伤应激素物肠粘膜的保护作用，采用３０％ＴＢＳＡⅢ度烫伤大鼠模型，观察了腹腔注射ＡＴＰ－ＭｇＣｌ２复合液对回肠粘膜丙二醛含量及回肠组织形态学改变的影响。结果显示：烫伤后６－２４小时，ＭＤＡ含量明显升高，并伴有形态学病理改变。     

ATP-MgCl_2对缺血后肝组织保护作用的研究

研究ATP-MgCl_2对缺血后肝组织的作用。方法:家兔全肝缺血30分钟后,分别给予生理盐水、ATP和ATP-MgCl_2处理,术后第1天,第3天和第5天取血测定谷丙转氨酶(ALT)、乳酸脱氢酶(LDH)和碱性磷酸酶(ALP),并分别检测各组肝组织学的改变。结果:术后第1天ATP-MgCl_2组ALT明显低于对照组(P<0.05),而ATP组与对照组相比无显著差别:ATP-MgCl_2及ATP组的LDH和ALP与对照组相比无显著差别。术后24小时超微结构示对照组肝细胞明显水肿、细胞器严重损伤和血窦内微小血栓;而ATP-MgCl_2组细胞轻度水肿,细胞器基本正常,血窦内无微小血栓。结论:ATP-MgCl_2对缺血肝组织确有保护作用,其机制可能是通过改善微循环和减轻细胞损伤而起作用。     

小剂量多巴胺对烫伤大鼠休克期肠粘膜的保护作用

目的　观察小剂量多巴胺对严重烫伤大鼠休克期肠粘膜机械屏障的保护作用。方法　大鼠预置心导管 ,30 %Ⅲ度烫伤后静脉复苏。观察大鼠常规治疗 (对照组 )和小剂量多巴胺 (3μg·kg-1·min-1)持续给药后 ,血清中二胺氧化酶 (DAO)、丙二醛 (MDA)及乳酸水平的变化 ,对肠道的病理学改变进行评分。　结果　多巴胺治疗组大鼠休克期一般情况明显好于对照组 ,小剂量多巴胺能显著降低严重烫伤大鼠血清中的乳酸、MDA、DAO水平 ,以伤后 3～ 12h明显 ;多巴胺治疗组大鼠回肠病理学评分明显优于对照组。　结论　小剂量多巴胺对严重烫伤大鼠休克期肠粘膜机械屏障有明显的保护作用。     

锌—金属硫蛋白对大鼠皮肤烫伤创面的影响

目的 研究Wistar大鼠深Ⅱ度烧伤后皮肤活力的下降与脂质过氧化反应的关系。方法 以氧耗量、琥珀酸脱氢酶、Schiff’s碱及创面愈合时间为指标,以金属硫蛋白作为保护剂外用于烫伤创面,分别采用空白对照及5×10^-6mol/L,1×10^-5mol/L两种浓度,测定伤后8,24,48h各项指标的变化。结果 皮肤氧耗量、琥珀酸脱氢酶活性下降,Schiffs碱含量明显升高。应用金属硫蛋白保护后,皮肤活性（氧耗及琥珀酸脱氢酶含量）均显著高于对照组（P＜0．05或P＜0．01）,同时Schiff’s碱含量下降（P＜0．05或P＜0．01）,创面愈合时间平均提前2天。结论 烫伤组织损伤与脂质过氧化反应有一定的关系,而金属硫蛋白有一定保护作用。     

CSH、SOD和ATP-MgCl_2对静脉皮瓣成活的影响

在兔胸腹部以胸腹壁静脉为轴形成4cm×6cm的静脉皮瓣。经静脉注射GSH,SOD,ATP-Mg-Cl_2,分别观察这三种药物对静脉皮瓣成活的影响。结果表明这三种药物使用后静脉皮瓣成活面积百分率分别为:GSH组86.56％、SOD组85.52％、ATP-mgcl2组76.25％,均显著高于对照组68.75％。文中对这三种药物提高静脉皮瓣成活面积的机制进行了探讨。     

锌-金属硫蛋白对大鼠皮肤烫伤创面的影响

目的研究 Wistar 大鼠深Ⅱ度烧伤后皮肤活力的下降与脂质过氧化反应的关系。方法以氧耗量、琥珀酸脱氢酶、Schiff's 碱及创面愈合时间为指标,以金属硫蛋白作为保护剂外用于烫伤创面,分别采用空白对照及5×10~(-6)mol/L,1×10~(-5) mol/L 两种浓度,测定伤后8,24,48h 各项指标的变化。结果皮肤氧耗量、琥珀酸脱氢酶活性下降,Schiffs 碱含量明显升高。应用金属硫蛋白保护后,皮肤活性(氧耗及琥珀酸脱氢酶含量)均显著高于对照组(P<0.05或 P<0.01),同时Schiff's 碱含量下降(P<0.05或 P<0.01),创面愈合时间平均提前2天。结论烫伤组织损伤与脂质过氧化反应有一定的关系,而金属硫蛋白有一定保护作用。     

锌-金属硫蛋白对大鼠皮肤烫伤创面的影响

目的研究Ｗｉｓｔａｒ大鼠深Ⅱ度烧伤后皮肤活力的下降与脂质过氧化反应的关系。方法以氧耗量、琥珀酸脱氢酶、Ｓｃｈｉｆ’ｓ碱及创面愈合时间为指标,以金属硫蛋白作为保护剂外用于烫伤创面,分别采用空白对照及５×１０－６ｍｏｌ／Ｌ,１×１０－５ｍｏｌ／Ｌ两种浓度,测定伤后８,２４,４８ｈ各项指标的变化。结果皮肤氧耗量、琥珀酸脱氢酶活性下降,Ｓｃｈｉｆｓ碱含量明显升高。应用金属硫蛋白保护后,皮肤活性（氧耗及琥珀酸脱氢酶含量）均显著高于对照组（Ｐ＜０．０５或Ｐ＜０．０１）,同时Ｓｃｈｉｆ’ｓ碱含量下降（Ｐ＜０．０５或Ｐ＜０．０１）,创面愈合时间平均提前２天。结论烫伤组织损伤与脂质过氧化反应有一定的关系,而金属硫蛋白有一定保护作用。     

严重烫伤大鼠肠粘膜通透性改变及其机理

采用~(99m)Tc-DTPA 血至肠腔清除率定量测定方法,观察大鼠严重烫伤后肠粘膜通透性的变化规律及血小板活化因子(PAF)对其产生的影响,以探讨严重烫伤后肠粘膜屏障功能损害的病理生理过程及机理。结果表明:严重烫伤后肠粘膜通透性显著升高,与肠组织 PAF 含量升高呈显著正相关(r=0.94,P<0.01),PAF 拮抗剂治疗能明显降低肠粘膜通透性。提示,PAF 是导致严重烫伤后肠粘膜通透性升高的重要因素之一。     

脂质过氧化抑制剂对大鼠肾脏低温保存和移植的保护作用

目的：探讨脂质过氧化反应对肾脏低温保存和移植的影响及其作用机制。方法：对大鼠肾脏低温保存和移植前进行脂质过氧化抑制预处理,观察移植肾脏功能和形态的变化,肾组织丙二醛（MDA）含量及白细胞介素－2（IL－2）、细胞间粘附分子－1（ICAM－1）、诱导型一氧化氮合酶（iNOS)的表达水平。结果：与对照组相比,治疗组肾脏形态和功能的异常均减轻,IL－2、ICAM－1、iNOS的表达水平和MDA含量明显降低,结论脂质过氧化抑制剂可减轻细胞脂质过氧化反应,对移植肾脏的形态和功能起到保护作用。     

抗内毒素类脂A单克隆抗体对烧伤脓毒症大鼠的保护作用

采用我所研究制备的抗内毒素类脂 A 单克隆抗体(mAb)观察了其对攻菌后动物的保护作用,并采用30%Ⅲ度 TBSA 烧伤大鼠模型注射内毒素,模拟临床烧伤脓毒症,旨在为临床防治提供理论依据。实验动物分烧毒组、治疗组及对照组,于伤后不同时相点观察血浆 LPS、TNF 的动态变化,同时作内脏的光镜及电镜形态学检查。结果表明:mAb 除在体外可与多种 G~-杆菌及纯化的内毒素反应外,细菌攻击前后注入 mAb 均能有效地提高感染动物的存活率,并可明显降低模拟烧伤脓毒症大鼠血中内毒素,减少 TNF 的分泌。光、电镜观察证实,可减轻机体的损害效应。提示:抗类脂 A 单克隆抗体是一种有效的治疗烧伤脓毒症的免疫制剂。     

脂质过氧化抑制剂对大鼠肾脏低温保存的保护作用

目的　探讨脂质过氧化抑制剂预处理对大鼠肾脏低温保存的作用及其机制。方法　对低温保存的大鼠肾脏进行脂质过氧化抑制剂U74 0 0 6F的预处理 ,观察肾组织中脂质过氧化代谢产物丙二醛含量及诱导型一氧化氮合酶表达水平的变化。结果　U74 0 0 6F预处理可降低肾组织氧化反应水平 ,减少诱导性一氧化氮合酶的表达。结论　U74 0 0 6F预处理通过抑制细胞脂质过氧化减轻氧化反应和细胞因子带来的损伤 ,对低温保存的肾脏起到保护作用     

抗内毒素类脂A单克隆抗体对烧伤脓毒症大鼠的保护作用

采用我所研究制备的抗内毒素类脂Ａ单克隆抗体（ｍＡｂ）观察了其对攻菌后动物的保护作用，并采用３０％Ⅲ度ＴＢＳＡ烧伤大鼠模型注射内毒素，模拟临床烧伤脓毒症，旨在为临床防治提供理论依据。实验动物分烧毒组、治疗组及对照组，于伤后不同时相点观察血浆ＬＰＳ、ＴＮＦ的动态变化，同时作内脏的光镜及电镜形态学检查。结果表明：ｍＡｂ除在体外可与多种Ｇ－杆菌及纯化的内毒素反应外，细菌攻击前后注入ｍＡｂ均能有效地提高感染动物的存活率，并可明显降低模拟烧伤脓毒症大鼠血中内毒素，减少ＴＮＦ的分泌。光、电镜观察证实，可减轻机体的损害效应。提示：抗类脂Ａ单克隆抗体是一种有效的治疗烧伤脓毒症的免疫制剂。     

Acute phase effects of ATP-MgCl<Subscript>2</Subscript> on experimental spinal cord injury

The purpose of this study was to study the acute phase effects of adenosine triphosphate (ATP)-MgCl₂ on experimental spinal cord clip compression injury. Spinal cord clip compression injury was performed on 36 albino Wistar rats. The rats were divided into five groups. T4–T8 total laminectomy was performed on all rats. Group 1: sham-operated group. Group 2: clip compression group. In group 3, ATP-MgCl₂ (100 μmol/kg) was given 2 min before the "clip compression injury." In group 4, ATP-MgCl₂ (100 μmol/kg) was given 5 min after the clip compression injury. In group 5, ATP MgC1₂ (100 μmol/kg) was administered 8 h after the injury. The spinal cords were excised for a length of 2 cm and deep frozen at –76°C. Tissue malondialdehyde (MDA) levels were used to determine the effects of ATP-MgCl₂ on spinal cord lipid peroxidation. In the groups in which ATP MgCl₂ was administered after the clip compression injury (groups 4 and 5), the decrease in spinal cord MDA levels was statistically significant when compared with those of the injury group (group 2). Although MDA levels of group 4 were lower than those of group 5, this difference was not statistically significant. Administration of the ATP-MgCl₂ before the clip compression injury (in group 3) did not have a statistically significant effect on lipid peroxidation when compared with the injury group (group 2). In this study, we found that ATP-MgCl₂ has decreased lipid peroxidation in spinal cord injury and protected the spinal cord from secondary injury after the trauma. We concluded that ATP-MgCl₂ may be used in the treatment of spinal cord injuries in conjunction with the other treatment modalities, but further investigations are mandatory. Electronic Publication     

Protective effect of deferoxamine on experimental spinal cord injury in rat

Objective

To observe the protective effect of deferoxamine on experimental spinal cord injury (SCI) in rats.

Methods

Sprague-Dawley rats were randomly divided into the following four groups. Control group: rats were performed laminectomy only; SCI group: rats were performed laminectomy with SCI; DFO group: rats were injected intraperitoneally a bolus of 100 mg/kg deferoxamine after SCI; vehicle group: rats were injected intraperitoneally 0.9% saline after SCI. The SCI of animal model was made by using a modified Allen's method on T₁₀. Six rats of each group were sacrificed at 4 h after injured, and the levels of free iron and malondialdehyde (MDA) of involved spinal cord segments were measured by bleomycin assay and the thiobarbituric acid (TBA) separately. The recovery of function was assessed by Modified Tarlov's scale and inclined plane method at 7, 14, 21 d after SCI. The histologic changes of the damaged spinal cord were also examined at 7 d after SCI.

Results

Following SCI, the levels of free iron and MDA were increased significantly and the Modified Tarlov's score and inclined plane angles decreased in SCI group and vehicle group. In DFO group, the levels of free iron and MDA were not increased, but the Modified Tarlov's score and inclined plane angles decreased, the histological findings were improved as well.

Conclusion

Deferoxamine can reduce the levels of free iron and lipid peroxidation, and improve the hind limb functional status of rats with spinal cord injury.     

脐带间充质干细胞对重度烧伤大鼠肾脏保护作用的研究

目的：观察脐带间充质干细胞（UCMSCs）移植对大鼠严重烧伤后肾脏损伤的影响,为干细胞应用于烧伤后的脏器保护研究奠定基础。方法：获取并分离培养孕大鼠UCMSCs并用流式细胞技术鉴定细胞表面抗原。48只SD大鼠随机分为4组：正常对照组（n=12）、生理盐水组（n=12）、乌司他丁组（n=12）和UCMSCs组（n=12）。正常对照组不作任何处理,立即活杀取材;其余3组制备20％TBSAIII度烧伤模型（98℃,12s）,于伤后48h分别静脉注射生理盐水0．1ml／g（生理盐水组）、乌司他丁1．6×105U／kg（乌司他丁组）和UCMSCs106／k（uCMSCs组）,于给药后7、14d观察大鼠肾脏组织病理学,免疫组化法观察组织凋亡相关蛋白Bcl-2的表达,并进行血尿素氮（BUN）、肌酐（cr）水平的测定。结果：烧伤后7、14d的组织病理学观察显示,干细胞移植后的大鼠烧伤后肾脏组织充血、肿胀等病理学改变较乌司他丁组及生理盐水组有所减轻,随时间延长减轻更加明显;免疫组化观察显示UCMSCs组伤后7d和14d肾组织中Bcl-2的表达较乌司他丁组和生理盐水组明显增多,表明肾组织抗凋亡能力增强。大鼠烧伤后BUN和Cr均较正常对照组显著升高。乌司他丁治疗组除14dBUN较生理盐水组升高外,其余时间BUN和Cr均明显下降。UCMSCs组伤后7和14d两肾功能指标均明显下降,与生理盐水组和乌司他丁组比较差异均有显著性（P〈0．05）,显示干细胞治疗对肾功能有明显改善作用。结论：UC—MSCs移植可有效减轻重度烧伤后大鼠‘肾脏组织的损伤并改善肾脏功能。     

Effects of Ligustrazine on pulmonary damage in rats following scald injury

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.