骨髓细胞参与甘油引起的小鼠急性肾小管坏死修复的实验观察

目的：观察骨髓来源的细胞能否分化成肾小管上皮细胞。方法：15只绿色荧光蛋白（GFP）标记的C57BL／6转基因小鼠提供骨髓细胞，64只同种无荧光标记的C57BL／6小鼠随机分为正常对照组（N组）、全身照射组（TBI组）、骨髓移植组（BMT组）、骨髓移植＋甘油注射组（B＋G组），每组16只。各组小鼠于不同时间点取血检测血常规、尿素氮及血肌酐，并取肾行H-E染色检查肾脏病理变化。流式细胞仪可以明确受体鼠骨髓细胞中CFP阳性细胞的比例，利用荧光显微镜及激光共聚焦显微镜采用荧光组织化学、免疫组织化学等方法观察GFP阳性细胞在受体鼠肾脏的分布及数量。结果：致死剂量^60Co照射虽然引起血常规三系减少，但并未对肾脏的组织结构及功能造成损伤。BMT组受体鼠在骨髓移植后第56天、84天时，肾小管中有少量GFP阳性细胞的存在，B＋G组受体鼠于上述同样时间点时肾小管中的GFP阳性细胞增多。激光共聚焦显微镜进一步证实了这些GFP阳性细胞位于肾小管上皮，并且荧光组织化学显示，这些GFP阳性细胞表达肾小管上皮细胞特异性功能蛋白Megalin。结论：骨髓细胞可以向肾小管上皮细胞分化．参与肾小管上皮细胞的更新。并且损伤可以使骨髓细胞的肾向分化率增加。     

FIZZ1在ApoE基因敲除鼠动脉粥样斑块中的表达

背景 FIZZ1是一种与炎症相关的缺氧诱导的有丝分裂因子,在肺部疾病缺氧状态下具有刺激肺动脉平滑肌细胞增殖等作用. 目的 探讨FIZZ1在ApoE基因敲除鼠粥样斑块表达情况及其对平滑肌细胞增殖的影响.方法 应用C57BL/6J ApoE基因敲除鼠构建动脉血管粥样硬化模型并与普通C57BL/6J野生型小鼠进行对照研究,通过对动脉血管HE染色及FIZZ1免疫检测斑块FIZZ1表达,同时给以不同浓度 FIZZ1刺激培养的平滑肌细胞,MTT法测定FIZZ1对平滑肌细胞增殖的影响.结果 ApoE基因敲除鼠高脂饲养24周后,主动脉根部明显形成动脉粥样硬化,斑块体积较大,免疫组化可见FIZZ1在粥样硬化斑块内明显表达,同龄野生型C57BL/6J鼠血管壁内,未见FIZZ1表达,重组FIZZ1能促进体外培养的平滑肌细胞增殖(与对照组比较,差别具有统计学意义,P＜0.05).结论 C57BL/6J野生型小鼠正常血管不表达FIZZ1,C57BL/6J ApoE基因敲除鼠粥样斑块表达FIZZ1,FIZZ1具有促进平滑肌细胞增殖的作用,提示其可能在动脉粥样硬化进展中起一定的作用.     

供体骨髓来源干细胞在骨髓嵌合小鼠肠上皮中定植和分化研究

目的 观察骨髓移植后供体骨髓来源干细胞（bone marrow derived stem cells，BMDSCs）是否能够在受体肠上皮中定植并分化为肠上皮细胞。方法 使用密度为1．073g／mL的Percoll分离GFP转基因小鼠的骨髓有核细胞。利用^60Co放射源对C57BL／6小鼠进行10Gy致死剂量照射，照射后4h经尾静脉移植绿色荧光蛋白（green fluorescence protein，GFP）转基因小鼠骨髓细胞建立嵌合小鼠模型，移植后1月和6月取小肠标本石蜡包埋。使用GFP抗体鉴定GFP阳性供体细胞在小肠上皮的表达情况，并使用GFP抗体和细胞角蛋白（PCK）抗体进行双标以判断BMDSCs是否分化上皮细胞，同时结合绒毛蛋白（Villin）和GFP的免疫荧光双标及连续切片染色肠道特异转录因子CDX2和GFP来分析骨髓来源细胞是否分化为肠道功能性上皮细胞。结果供体骨髓来源细胞在嵌合鼠的骨髓和小肠上皮层中均有定植，且小肠上皮中GFP阳性细胞能够同时表达PCK、Villin和CDX2。结论 供体骨髓来源干细胞可以在骨髓嵌合小鼠的肠上皮定植，并分化为具有正常功能的小肠上皮细胞。     

动脉粥样硬化斑块内FIZZ1表达促进平滑肌细胞清道夫受体-A上调

目的探讨ApoE基因敲除鼠动脉粥样硬化斑块内FIZZ1表达情况及其对平滑肌细胞清道夫受体A(SR-A)表达的影响.方法C57BL/6J ApoE基因敲除鼠及C57BL/6J野生型小鼠各9只,分别喂养高脂饲料及普通饲料,24周后处死小鼠,石蜡包埋血管后做连续切片,行HE染色及FIZZ1免疫组化.用氧化型低密度脂蛋白(ox-LDL)以及终浓度分别为3×10-6mmol/L、9×10-6mmol/L、2.7×10-5mmol/L的FIZZ1刺激培养的平滑肌细胞,激光共聚焦显微镜确认SR-A表达后,流式细胞术检测FIZZ1对ox-LDL诱导的平滑肌细胞SR-A表达的影响.结果ApoE基因敲除鼠高脂饲养24周后,主动脉根部明显形成动脉粥样硬化,可见FIZZ1在动脉粥样硬化斑块内明显表达,同龄野生型C57BL/6J鼠正常血管壁内,未见FIZZ1表达,重组FIZZ1能明显促进ox-LDL诱导的平滑肌细胞SR-A表达(与对照组比较,P<0.01).结论C57BL/6J野生型小鼠正常血管不表达FIZZ1,C57BL/6JApoE基因敲除鼠动脉粥样斑块表达FIZZ1,FIZZ1促进ox-LDL诱导的平滑肌细胞SR-A表达,提示FIZZ1可能在ApoE基因敲除鼠动脉粥样硬化进展中起一定的促进作用.     

MSCs对辐射诱导C57BL/6J鼠胸腺瘤的抑制作用

目的 观察MSCs对辐射诱导C57BL/6J鼠胸腺瘤模型的抑制作用.方法 无菌分离C57BL/6J鼠股骨,全骨髓贴壁法培养MSCs.将实验分为三组:正常组对照组、辐射组及MSCs治疗组.应用深部X线放射治疗机对C57BL/6J鼠进行全身照射,1次/w,共4次.末次照射结束后第二日,治疗组小鼠经尾静脉回输MSCs,1次/w,共2次.6个月后无菌取出各组的C57BL/6J鼠胸腺,研磨制成单细胞悬液,流式细胞仪检测CD45表达.提取组织RNA,利用RT-PCR检测caspase-3表达.结果 MSCs对辐射诱导C57 BL/6J鼠胸腺瘤模型CD45+的表达,治疗组CD45阳性百分率高于模型组(P＜0.01),模型组CD45阳性百分率低于正常对照组(P＞0.05).MSCs对辐射诱导C57BL/6J鼠胸腺瘤模型胸腺caspase-3的表达,治疗组Caspase-3 mRNA表达高于模型组(P＜0.05),高于正常对照组(P＜0.05),模型组Caspase-3mRNA表达接近于正常对照组(P＞0.05).结论 MSCs对辐射诱导C57BL/6J鼠胸腺瘤模型有抑制作用.     

骨髓间充质干细胞在小鼠肝脏局部分化为肝细胞的实验研究

目的 探讨小鼠骨髓间充质干细胞（bone marrow mesenchymal stem cells，BMSCs）在肝内分化为肝细胞的可行性。方法腹腔注射丙烯醇致雌性C57BL／6小鼠全肝损伤后局部接受雄性同品系绿色荧光蛋白（green fluorescence protein，GFP）转基因小鼠骨髓间充质干细胞移植。移植后3周取骨髓嵌合小鼠肝脏做冰冻切片，荧光显微镜下观察GFP阳性细胞在肝内分布，石蜡切片行GFP抗体和白蛋白（albumin，Alb）抗体免疫组化双标法检测GFP阳性细胞在受体小鼠肝内的分化情况。结果移植后3周小鼠肝内可见GFP阳性细胞，并可见GFP和Alb双阳性细胞。结论异体骨髓间充质干细胞可在小鼠肝内分化为表达Alb的肝细胞，为肝组织的再生和修复提供了新思路，显示了其在肝病治疗中的应用潜力。     

IFN-γ和Toll样受体在弓形虫感染诱发的肾病中的作用

IFN-γ可抑制弓形虫在肾脏等多种组织中的增殖，在免疫保护中具彳丁重要作用，但组织的炎性病变程度与虫体的数量往往不成比例。近来有研究显示Toll样受体家族（TLRs）参与了肾脏抗感染的先天免疫机制；炎性病变的肾小管上皮细胞TLR2和TLR4mRNA合成明显增加；TLR2和髓样分化因子88（MyD88，一种重要的胞内转接蛋白）在宿主抗真菌、抗细菌和抗弓形虫感染的保护机制中起重要作用。为了探求弓形虫感染与肾脏病变的病理联系，最近日本干叶大学Kudo等研究了IFN-γ和TLRs对弓形虫感染小鼠肾脏的免疫保护作用。以弱毒的成囊型Fukaya株弓形虫经口感染不同型别小鼠，被感染小鼠有6种，野生型（WT）BALB／c小鼠，野生型C57BL／6小鼠，IFN-7基因敲除（GKO）BALB／c小鼠，IFN-γ基因敲除C57BL／6小鼠，TLR2缺陷C57BL／6小鼠和TLR4缺陷C57BL／6小鼠。     

FIZZ1在ApoE基因敲除鼠动脉粥样斑块中的表达

背景FIZZ1是一种与炎症相关的缺氧诱导的有丝分裂因子,在肺部疾病缺氧状态下具有刺激肺动脉平滑肌细胞增殖等作用。目的探讨FIZZ1在ApoE基因敲除鼠粥样斑块表达情况及其对平滑肌细胞增殖的影响。方法应用C57BL/6J ApoE基因敲除鼠构建动脉血管粥样硬化模型并与普通C57BL/6J野生型小鼠进行对照研究,通过对动脉血管HE染色及FIZZ1免疫检测斑块FIZZ1表达,同时给以不同浓度FIZZ1刺激培养的平滑肌细胞,MTT法测定FIZZ1对平滑肌细胞增殖的影响。结果ApoE基因敲除鼠高脂饲养24周后,主动脉根部明显形成动脉粥样硬化,斑块体积较大,免疫组化可见FIZZ1在粥样硬化斑块内明显表达,同龄野生型C57BL/6J鼠血管壁内,未见FIZZ1表达,重组FIZZ1能促进体外培养的平滑肌细胞增殖(与对照组比较,差别具有统计学意义,P<0.05)。结论C57BL/6J野生型小鼠正常血管不表达FIZZ1,C57BL/6J ApoE基因敲除鼠粥样斑块表达FIZZ1,FIZZ1具有促进平滑肌细胞增殖的作用,提示其可能在动脉粥样硬化进展中起一定的作用。     

丙丁酚可干预小鼠动脉粥样硬化病变并调节B类I型清道夫受体的表达

目的研究丙丁酚对高脂高胆固醇饲养的载脂蛋白E基因敲除小鼠和C57BL6／J小鼠血脂及动脉粥样硬化病变的影响，以及肝脏B类Ⅰ型清道夫受体和PPARγ表达的变化。方法分别随机将20只载脂蛋白E^-/^-小鼠和20只C57BL6／J小鼠分为载脂蛋白E^-／^-高脂组和载脂蛋白E^-/^-高脂＋0．5％丙丁酚组。     

NOX4和eNOS在小鼠慢性缺氧肺血管重塑中的表达及意义

目的观察内皮型一氧化氮合酶（eNOS）和NOX4在小鼠慢性缺氧肺动脉高压形成过程中的改变。方法用HE染色法和免疫组织化学法观察C57BL／6J小鼠在常氧和慢性持续缺氧（10±0．5％O2）1、3、7、14d后肺血管的改变及非肌型小血管d．SMA和eNOS蛋白表达的改变。用Real TimePCR法检测各组小鼠肺组织中eNOS和NOX4mRNA的含量。结果C57BL／6J小鼠慢性缺氧后肺小动脉血管管壁增厚、肺泡内肺动脉d—SMA表达增加,肺组织eNOS和NOXdmRNA以及肺动脉内皮细胞eNOS蛋白的表达随缺氧时间延长进行性升高。结论eNOS和NOX4可能在慢性缺氧肺动脉高压的发病机制中发挥重要作用。     

Hematopoietic origin of glomerular mesangial cells

It was recently reported that crude bone marrow cells have the ability to differentiate into glomerular mesangial cells. However, the exact nature of the engrafting cells in the bone marrow was not known. We tested the hypothesis that hematopoietic stem cells are capable of reconstituting the mesangial cells by transplanting a clonal population of cells derived from a single stem cell. We cultured Lin(-), Sca-1(+), c-kit(+), CD34(-) bone marrow cells from transgenic enhanced green fluorescent protein (EGFP) mice (C57BL/6-Ly-5.2 background) individually for 1 week in the presence of interleukin-11 and steel factor. We then transplanted viable clones individually into lethally irradiated C57BL/6-Ly-5.1 mice. Kidneys from 5 recipient mice showing high levels (60%-90%) of multilineage hematopoietic reconstitution were examined 2 to 6 months later, using differential interference contrast and epifluorescence microscopy. EGFP(+) cells with a morphology characteristic of mesangial cells were evident within the glomeruli. Transplantation of 100 noncultured Lin(-), Sca-1(+), c-kit(+), CD34(-) bone marrow cells also generated mesangial cells. Cultured EGFP(+) glomerular cells from recipient mice contracted in response to angiotensin II. EGFP(+) mesangial cells seen in male-to-male transplants revealed only one Y-chromosome. These data demonstrate that a single hematopoietic stem cell is capable of differentiating into glomerular mesangial cells and that the process does not involve cell fusion.     

Genetic control of natural resistance to Trypanosoma rhodesiense: transfer of resistance with bone marrow or spleen cells

Inbred strains of mice differ greatly in their innate resistance to Trypanosoma rhodesiense, the etiologic agent of African sleeping sickness. BALB/c mice are very susceptible to this organism, whereas C57BL/6 mice are highly resistant. This difference is regulated by at least three distinct genes. An adoptive transfer study was performed in order to determine the tissue site of expression of these genes. Three inbred mouse strains (C57BL/6J, C3H.SW/SnJ, and BALB.B) that differ in resistance to T. rhodesiense, but are histocompatible at the H-2 locus, were used in the study. The adoptive transfer of normal bone marrow cells from C57BL/6J (resistant) mice into X-irradiated BALB.B (susceptible) mice rendered the recipient mice resistant to a subsequent experimental challenge with T. rhodesiense. Conversely, the transfer of bone marrow cells from BALB.B mice into irradiated C57BL/6J mice rendered the latter mice susceptible. Resistance could also be adoptively transferred from C57BL/6J mice to a second susceptible strain, C3H.SW/SnJ, by using either bone marrow or spleen cells. These findings demonstrate that although multiple genes control innate resistance to T. rhodesiense, all or most of these genes appear to control the development or function of cells whose progenitors reside in the spleen and bone marrow.     

Nonmyeloablative conditioning is sufficient to allow engraftment of EGFP-expressing bone marrow and subsequent acceptance of EGFP-transgenic skin grafts in mice

Immunologic reactions against gene therapy products may prove to be a frequent problem in clinical gene therapy protocols. Enhanced green fluorescence protein (EGFP) is commonly used as a marker in gene transfer protocols, and immune responses against EGFP-expressing cells have been documented. The present study was designed to investigate the effect of a pharmacologic, nonmyeloablative, conditioning regimen on the development of EGFP+ donor/recipient mixed bone marrow chimerism and ensuing tolerance to EGFP-expressing transplants. To this end, C57BL/6J (B6) mice were treated with soluble formulations of either busulfan (Busulfex) or the closely related compound treosulfan, followed by transplantation of bone marrow cells from EGFP-transgenic (B6-EGFP.Tg) donor mice. Such conditioning regimens resulted in long-term persistence of donor EGFP+ cells among various hematopoietic lineages from blood, bone marrow, and thymus. Stable hematopoietic chimeras transplanted at 10 to 17 weeks after bone marrow transplantation (BMT) with B6-EGFP.Tg skin grafts all accepted their transplants, whereas non-EGFP chimeric B6 control animals were able to mount rejection of the EGFP+ B6 skin grafts. Control third-party grafts from major histocompatibility complex (MHC)-mismatched mice were rejected within 20 days, indicating that acceptance of EGFP-expressing skin grafts was the result of specific immune tolerance induction by the transplantation of EGFP-transgenic bone marrow. Long-term tolerance to EGFP in chimeric recipients was confirmed by the absence of anti-EGFP-reactive T cells and antibodies. These results broaden the therapeutic potential for using hematopoietic molecular chimerism in nonmyeloablated recipients as a means of preventing rejection of genetically modified cells.     

Morphology and quantitative composition of hematopoietic cells in murine bone marrow and spleen of healthy subjects

Laboratory mice play an outstanding role in modeling human development and disease. In contrast to human leukemia, the spleen is involved in almost all cases, and the bone marrow is only variably involved in murine models. Although mice have been used for medical research for over 100 years, there are only few reports with a small number of cases looking at morphology and quantitative composition of murine hematopoietic cells in the bone marrow of non-transplanted animals of most strains. To our knowledge, there is not even a single report describing the splenogram in C57BL/6J mice, one of the most commonly used strains for medical research. The present study illustrates the morphology of the hematopoietic cells in the bone marrow and spleen of non-treated C57BL/6J mice and establishes the murine myelogram from the largest healthy C57BL/6J cohort reported to date. Furthermore, we present the first murine splenogram described for C57BL/6J mice. Our study supports the acceptance of the presence of >5 % blast cells as providing clear evidence of abnormality in bone marrow like in humans. In addition, we are the first to show <1 % blast cells in the normal spleen. Interestingly, classical dysplastic changes were rare in normal healthy mice. Our study of the bone marrow and spleen of healthy non-transplanted animals provides reference ranges of each cell type and for the myeloid/erythroid ratio, which can be used to interpret preclinical gene therapy data, leukemogenesis, and hematopoiesis studies, and may improve the quality of such analyses.     

小鼠骨髓源性肥大细胞的培养及鉴定

目的：在体外利用小鼠骨髓干细胞诱导获得高纯度的肥大细胞。方法：从小鼠股骨获得骨髓细胞，放入含10％胎牛血清的RPMI1640培养基中，加入不同浓度的刺激因子，即IL-3和SCF各分别为10ng／ml、15ng／ml、20ng／ml，放入CO2培养箱中培养4周，用免疫组化观察CD117的表达，用流式细胞术检测CD117和FceR1α双阳性细胞的比例，用甲苯胺蓝染色法观察细胞的成熟度，并与较常用的肥大细胞系P815做比较。结果：培养获得的肥大细胞，其中IL-3和SCF分别为10ng／ml和15ng／ml时均可在4周后得到纯度大于95％的CD117和FcεRIα双阳性肥大细胞，而20ng／ml时FcεRIα的表达却有所降低，双阳性细胞仅达90％，而P815细胞系表达FcεRIα的比例很低。免疫组化发现培养获得的细胞大部分均表达CD117。甲苯胺蓝染色发现培养获得的细胞核被染成深蓝色，胞浆中布满大量紫红色的颗粒，呈现肥大细胞的典型特征。而P815却少见典型的紫红色异染颗粒。结论：用IL-3和SCF各10ng／ml可在体外成功培养获得高纯度的小鼠骨髓源性肥大细胞，且其在表型和成熟度方面均好于P815细胞系。     

Intra-bone marrow injection of bone marrow and cord blood cells: an alternative way of transplantation associated with a higher seeding efficiency

OBJECTIVE: Intravenous (IV) injection is currently the normal method for transplanting hematopoietic cells. However, the problem of seeding efficiency and homing is relevant especially when a limited number of stem cells is available. Intra-bone marrow (IBM) injection of bone marrow cells (BMCs) may overcome this problem. MATERIALS AND METHODS: Irradiated (750 cGy) C57BL/6J mice were transplanted with 1 x 10(5) BMCs harvested from transgenic mice expressing an enhanced version of the green fluorescent protein (EGFP+) via IBM or with 1 x 10(6) EGFP+ BMCs via IV. Irradiated (320 cGy) NOD/SCID mice were transplanted with 1 x 10(6) human cord blood (CB) cells via IBM or with 1 x 10(7) human CB cells via IV. RESULTS: In C57BL/6J mice after 90 days, the fraction of EGFP+ cells harvested was 37% and 53% in IV-treated and IBM-treated (contralateral tibia and femur in the IBM) mice, respectively: the expansion folds were 114 and 1760, respectively. In NOD/SCID mice, the percentages of CD45+ cells and CD45+/CD34+ cells were, at 30 days, 3.3% and 0.3% in IV-treated mice, and 4.4% and 1.1% in IBM-treated mice. At 60 days, the percentages of CD45+ cells and CD45+/CD34+ cells were 2.1% and 0.3% in IV-treated mice and 1.4% and 0.4% in IBM-treated mice. At day 90 the percentages of CD45+ cells and CD45+/CD34+ cells were 3% and 0.3% in IV-treated mice and 2.3% and 0.4% in IBM-treated mice. CONCLUSION: Our data demonstrate that IBM transplantation is associated with a seeding efficiency 15 times greater than IV transplantation. IBM transplantation may improve the results of transplant and may be useful in several settings: 1) when a limited number of hematopoietic progenitors are available; and 2) in experiments aiming to place in the bone marrow stem cells of other lineages (CNS, muscle, etc.).     

Reduction of lethal graft-versus-host disease: transplantation of cultured murine bone marrow across minor histocompatibility differences

The murine bone marrow culture technique was used to prepare donor marrow for bone marrow transplantation across minor histocompatibility complex differences. Previous studies have shown that theta-positive cells are rapidly lost from such cultures and that transplantation of cultured marrow across major histocompatibility complex differences results in a delay in the development of lethal graft-v-host disease (GVHD). In this study, a total of 1 to 2 X 10(7) nonadherent cells (740 to 1560 CFUs [colony-forming units]) from three-day-old cultures were used as a source of donor marrow. Three strain combinations were evaluated; LP/J into C57BL/6; BIO.BR into CBA/J; and C57BL/6 into LP/J. Donor mice were immunized with recipient spleen cells prior to culture in order to increase the graft-v-host response. For LP/J marrow into C57BL/6 mice, 5 X 10(7) donor spleen cells transplanted along with the marrow were needed to induce lethal GVHD. However, lethal GVHD was seen without the addition of spleen cells for BIO.BR into CBA/J and C57BL/6 into LP/J strain combinations. Most animals receiving fresh marrow were dead of GVHD five weeks after transplantation. With the use of cultured marrow the three-month survival was 80%, 51%, and 93%, respectively, for LP/J into C57BL/6, BIO.BR into CBA/J, and C57BL/6 into LP/J strain combinations. Long-term donor engraftment in all recipient animals receiving cultured marrow was confirmed by analyzing hemoglobin polymorphisms between the strain combinations. These results demonstrate that in contrast to transplantation across major histocompatibility complex differences, the use of cultured cells for bone marrow transplantation across minor histocompatibility complex differences allows for engraftment while reducing the risk of lethal GVHD.     

三种品系小鼠对伴刀豆球蛋白A所致急性肝损伤的耐受性比较研究

目的：应用不同剂量伴刀豆球蛋白 A（ConA）诱导三种不同品系小鼠急性肝损伤,比较肝酶变化、死亡率和肝组织病理学变化。方法分别用6、12、20和30 mg·kg-1 ConA 处理 C57BL/6J、BABL/c 和 KM 小鼠,8 h 后对比观察急性肝损伤动物血清酶学及肝组织病理学变化情况。结果在6 mg·kg-1 ConA 的作用下,三个品系小鼠均被成功制造出急性肝损伤模型;在12 mg·kg-1 ConA 作用下,KM 小鼠血清 ALT 和AST 分别为（1006.8±12.1） U/L 和（1391.8±13.4）U/L,显著高于 BABL/c 小鼠[（75.7±0.5）U/L 和（284.7±23.4） U/L）和 C57BL/6J 小鼠（104.4±32.2）U/L 和（492.2±12.3）U/L,P 均〈0.05];同样,KM 小鼠肝指数和脾指数分别为（5.4±0.3）和（0.7±0.5）,均显著高于 BABL/c 小鼠[（5.2±0.4）和（0.6±0.3）和 C57BL/6J 小鼠（5.0±0.6）和（0.6±0.2）,P 均〈0.05];在20 mg·kg-1 ConA 作用下,三组小鼠血清 AST 和 ALT 水平无统计学差异,但 BABL/c 小鼠（4/10）和 C57BL/6J 小鼠（5/10）死亡率显著高于 KM 小鼠（1/10）;在30 mg·kg-1 ConA 作用下,三个品系小鼠死亡率均较高（KM 小鼠为30%,BABL/c 和C57BL/6J 小鼠均为100%）。结论不同品系的小鼠对 ConA 的耐受性不同,KM 小鼠对 ConA 的耐受性明显优于BABL/c 小鼠和 C57BL/6J 小鼠,且呈剂量依赖性。     

骨髓间充质干细胞对急性肺损伤大鼠氧化应激的影响

目的观察骨髓间充质干细胞对内毒素性急性肺损伤的保护作用及机制。方法健康4月龄SPF级雄性C57BL/6J小鼠8只,用于骨髓间充质干细胞分离培养;SPF级雄性SD大鼠90只,随机分成:正常对照组(A组);内毒素组(B组)、骨髓间充质干细胞高剂量组(C组)、骨髓间充质干细胞低剂量组(D组)、骨髓间充质干细胞对照组(E组)。于造模后6、24、72小时,处死动物,每个时间点6只。分别取肺组织,测定肺湿质量/干质量。检测肺组织中超氧化物歧化酶(SOD)活力和丙二醛(MDA)及髓过氧化物酶(MPO)含量。观察肺组织病理学改变。结果 LPS的24小时组死亡1只,两个骨髓间充质干细胞治疗组与模型组相比,肺组织SOD的活力明显增高,MDA和MPO含量显著降低(P<0.05);病理明显的改善,肺湿质量/干质量降低。正常对照组和骨髓间充质干细胞组相比,上述指标差异无统计学意义。结论骨髓间充质干细胞对内毒素性急性肺损伤有一定保护作用,其机制与抗氧化能力有关。不同种属骨髓间充质干细胞移植后,未见明显损伤。