逆转录PCR检测肝再生过程eNOS的基因表达

探讨ｅＮＯＳ基因表达对再生的影响。方法 以７０％肝切除制备大鼠肝再生模型，注射ＣＣｌ４和脾切除引起肝损伤和机体免疫功能低下。ＦＣＭ检测再生肝ＤＮＡ的复制，ＲＴ－ＰＣＲ检测ｅＮＯＳ的改变与再生肝ＤＮＡ复制的关系。结果 肝再生过程伴有ｅＮＯＳ的基因表达，ＣＣｌ４肝损害或切队脾脏后肝细胞ＤＮＡ复制的减少伴有ｅＮＯＳ基因表达的减少；ＣＣｌ４肝损害的同时切除脾脏ｅＮＯＳ的基因表达量与单独的ＣＣｌ４肝损伤组并     

内毒素诱生大鼠腹腔巨噬细胞IL-12 mRNA表达调控及大黄酸对其作用研究

应用ＲＴＰＣＲ及荧光探针标记技术观察大鼠腹腔巨噬细胞经内毒素活化后ＩＬ１２ｍＲＮＡ表达水平及细胞内信号传递系统和大黄酸对其调控作用。结果表明，内毒素能活化大鼠腹腔巨噬细胞使［Ｃａ２＋］ｉ水平及ＩＬ１２ｍＲＮＡ表达水平明显升高，并呈剂量依赖相关关系，随着ＬＰＳ剌激浓度的增加，ＩＬ１２ｍＲＮＡ表达水平及细胞内游离钙离子浓度逐渐增加。大黄酸能显著抑制ＬＰＳ活化的大鼠腹腔巨噬细胞ＩＬ１２ｍＲＮＡ表达水平及［Ｃａ２＋］ｉ的升高，亦呈剂量依赖相关关系，随着大黄酸浓度的增加ＩＬ１２ｍＲＮＡ表达水平及［Ｃａ２＋］ｉ逐渐降低。ＰＫＣ活化剂ＰＭＡ及Ａ２３１８７能显著提高ＩＬ１２ｍＲＮＡ的表达水平（与对照比较Ｐ＜０．００１，与ＬＰＳ组比较Ｐ＜０．０５）而ＰＫＣ抑制剂Ｃａｌ及ＳＰ能使经ＬＰＳ活化的大鼠腹腔巨噬细胞ＩＬ１２ｍＲＮＡ表达水平明显降低（与ＬＰＳ组比较Ｐ＜０．０１），大黄酸亦能显著抑制ＬＰＳ所至ＩＬ１２ｍＲＮＡ表达水平的升高。表明大鼠腹腔巨噬细胞经ＬＰＳ活化后其ＩＬ１２ｍＲＮＡ表达需经细胞内信号传递系统调控，大黄酸通过降低［Ｃａ２＋］ｉ使ＩＬ１２ｍＲＮＡ表达水平降低。     

白细胞介素10基因表达对肝再生过程的影响

探讨白细胞介素１０基因表达及脾脏对肝再生过程的影响。方法 通过大鼠７０％肝切除制备肝再生模型，以流式细胞仪检测肝细胞ＤＮＡ的复制，分子杂交显示ＩＬ－１０的基因表达，免疫组化以及形态测量学方法了解ＩＬ－１０在肝内的分布，经统计学分析判断肝损伤和切脾后ＩＬ－１０对肝再生的影响。     

腰椎间盘突出症髓核内一氧化氮和白介素-6的检测意义

目的：了解一氧化氮（ＮＯ）和白介素６（ＩＬ６）在腰椎间盘突出症患者髓核内的含量,并探讨其意义。方法：共对２８例３０个间隙Ｌ４,５和／或Ｌ５Ｓ１间隙椎间盘突出患者突出髓核取组织匀浆测定了ＮＯ、ＩＬ６的含量,以光密度法测定ＮＯ,并以夹心法ＥＬＩＳＡ测定ＩＬ６。结果：ＮＯ的含量为５１７３±６８４μｍｏｌ／Ｌ,ＩＬ６０１３±００１ｎｇ／Ｌ;ＮＯ和ＩＬ６的含量明显相关,但两者与ＮＯＳ（一氧化氮合酶）的含量无明显的相关性,Ｌ４,５与Ｌ５Ｓ１间隙ＮＯ的含量有显著性差异。结论：腰椎间盘自身可合成ＮＯ,ＮＯ的合成与椎间盘的退变有关。ＮＯ、ＩＬ６参与局部的炎症调节,其含量与临床症状密切相关;通过调控ＮＯ的合成可能有助于防治椎间盘的退变、突出,并控制其临床症状。     

PGE2和IL-2/IL-2R 在胃癌患者手术前后的动态变化和相互关系

目的　探讨胃癌患者外周血中白细胞介素２ （ＩＬ２）、白细胞介素２ 受体（ｓＩＬ２Ｒ） 水平及ＣＤ２５ 表达三者手术前后的动态变化情况和相互关系,以及前列腺素Ｅ２（ＰＧＥ２） 与ＩＬ２／ＩＬ２Ｒ系统的关系。方法　分别采用ＥＬＩＳＡ法、１２５ＩＲＩＡ法及免疫荧光法对５０ 例胃癌患者手术前后外周血中ＩＬ２、ｓＩＬ２Ｒ、ＰＧＥ２ 水平及ＣＤ２５ 表达进行检测。结果　胃癌患者手术前后外周血中ＩＬ２ 水平及ＣＤ２５ 表达均低于对照组,而ｓＩＬ２Ｒ与ＰＧＥ２ 水平均高于对照组;切除肿瘤后ＩＬ２ 水平及ＣＤ２５ 表达较术前升高,而ｓＩＬ２Ｒ及ＰＧＥ２ 水平较术前下降;６ 例术后发生肿瘤转移或复发的患者中,再次出现ＩＬ２ 水平及ＣＤ２５ 表达下降,而ｓＩＬ２Ｒ及ＰＧＥ２ 水平上升,胃癌患者术前ＩＬ２ 水平与术前ＰＧＥ２ 水平呈显著负相关,术前ｓＩＬ２Ｒ水平与ＩＬ２ 水平亦呈显著负相关。结论　ＰＧＥ２ 与ｓＩＬ２Ｒ 参与了胃癌患者术前存在的免疫抑制过程。非甾体抗炎药（ＮＳＡＩＤ）与外源性ＩＬ２ 联合应用以预防胃癌转移或复发理论上具有可行性。     

CsA、MPA和RPM对CD_(28)通路共刺激后淋巴细IL-4 mRNA表达的影响

目的　观察环孢素Ａ（ＣｓＡ） 、霉酚酸（ ＭＰＡ） 和雷帕霉素（ＲＰＭ） 对ＣＤ２８ 通路共刺激后淋巴细胞ＩＬ４ ｍ ＲＮＡ 表达的影响。　方法　以ＰＣＲ 扩增方法获得ＩＬ４ 特异的ｃＤＮＡ 片段,并将其克隆至ＰＧＥＭ３Ｚ 载体中。以此作为探针对ＲＴＰＣＲ 产物进行杂交定量,比较三种免疫抑制剂对ＣＤ２８通路共刺激后淋巴细胞ＩＬ４ ｍ ＲＮＡ 表达的影响。　结果　以抗ＣＤ３ ｍ Ａｂ ＋ 抗ＣＤ２８ ｍ Ａｂ 共刺激后,发现淋巴细胞稳定地表达ＩＬ４ ｍ ＲＮＡ;ＣｓＡ 和ＭＰＡ 未能抑制淋巴细胞ＩＬ４ ｍ ＲＮＡ 的表达,而ＲＰＭ则能产生显著抑制。　结论　ＲＰＭ 能抑制ＣＤ２８ 通路共刺激后ＩＬ４ ｍ ＲＮＡ 的表达,而ＣｓＡ 和ＭＰＡ对这一过程无抑制作用。     

淋巴细胞CD28通路活化后Th1/Th2细胞因子mRNA表达及CsA的抑制作用

采用ＲＴＰＣＲ方法，观察ＣＤ２８通路活化后淋巴细胞Ｔｈ１／Ｔｈ２细胞因子ｍＲＮＡ表达水平及ＣｓＡ的抑制作用。取正常人外周血淋巴细胞，培养过程中分别给予抗ＣＤ３ｍＡｂ单独刺激或抗ＣＤ３ｍＡｂ＋抗ＣＤ２８ｍＡｂ共同刺激。提取细胞总ＲＮＡ并逆转录成ｃＤＮＡ，对Ｔｈ１细胞因子（ＩＦＮγ、ＩＬ２）和Ｔｈ２细胞因子（ＩＬ４、ＩＬ１０）ｃＤＮＡ进行扩增。结果显示：共刺激信号可使Ｔｈ１细胞因子基因ｍＲＮＡ转录增加，且对ＣｓＡ的抑制作用产生抵抗；而对Ｔｈ２细胞因子则不产生明显影响。研究表明：ＣＤ２８共刺激信号主要增强淋巴细胞Ｔｈ１细胞因子基因ｍＲＮＡ表达，并可能参与其分化调节；这一活化通路不被ＣｓＡ阻断。     

动脉硬化闭塞症与血管内皮细胞活性因子关系的研究

目的　探讨动脉硬化闭塞症（ＡＳＯ） 与内皮素１（ＥＴ１） 、一氧化氮（ＮＯ） 等血管内皮细胞活性因子的相互关系。方法　选择９６ 例ＡＳＯ 患者，采用密度梯度法检测循环内皮细胞计数（ＣＥＣ），采用放射免疫测定法检测血浆ＥＴ１ 、血栓素Ｂ２（ＴＸＢ２）、６酮前列腺素Ｆ１α（６ＫＰＧＦ１α） ，降钙素基因相关肽（ＣＧＲＰ） 、血管紧张素Ⅱ（ＡＴⅡ）、肿瘤坏死因子（ＴＮＦ），采用酶联免疫检测细胞间粘附分子１（ＩＣＡＭ１）、Ｐ选择素（ＰＳ）。采用Ｇｒｉｓｓ 法检测血浆ＮＯ水平。结果　所有患者均存在高ＥＴ１、ＴＸＢ２ 、ＡＴⅡ、粘附分子、ＣＥＣ血症，存在低ＮＯ、ＣＧＲＰ、６ＫＰＧＦ１α血症，且以Ⅲ期病人最明显。结论　ＡＳＯ 的发生发展同血管内皮细胞活性因子密切相关，ＥＴ１、ＮＯ 等血管活性因子的检测有助于ＡＳＯ发病机制的探讨和病情严重程度的判别。     

肝硬变大鼠行部分肝叶切除术后枯否细胞DNA和RNA合成功能的变化

作者通过肝硬变大鼠模型，行部分肝叶切除术，动态观察再生肝脏Ｋｕｐｆｆｅｒ细胞ＤＮＡ和ＲＮＡ合成功能变化规律，探讨肝再生机制与肝细胞功能衰竭的关系。７０只健康的雄性Ｗｉｓｔａｒ大鼠，体重２２０－２５０ｇ，分为肝硬变大鼠部分肝叶切除术组（Ｃ－ＰＨ）．正常大鼠部分肝叶除术组（Ｎ－ＰＨ）和假手术组（ＳＯ）。Ｎ－ＰＨ组和Ｃ－ＰＨ组均切除大鼠肝脏的左叶和中叶。各组于不同时相用流式细胞仪测定Ｋｕｐｆｆｅｒ细胞的ＤＮＡ和ＲＮＡ含量。结果表明：Ｃ－ＰＨ组枯否氏细胞Ｇ２期和Ｍ期ＤＮＡ合成的高峰是在术后２４小时以后，明显落后于Ｎ－ＰＨ组；其Ｋｕｐｆｆｅｒ细胞增殖系数的峰值在术后４８小时，以后持续高于Ｎ－ＰＨ组和ＳＯ组，但其残肝的重量在术后１周时低于Ｎ－ＰＨ组；Ｋｕｐｆｆｅｒ细胞ＲＮＡ含量一直低于Ｎ－ＰＨ组和ＳＯ组，于术后一周时其ＲＮＡ合成的水平才恢复到术前的水平。作者认为，肝硬变大鼠行肝叶部分切除术后枯否氏细胞功能受抑制，其启动时间的推迟和再生周期的延长是造成术后肝细胞再生能力低下和肝细胞功能衰竭的一个重要原因。     

L-NIL对脓毒血症模型小鼠细胞能量代谢及存活率的影响

目的　观察诱导型一氧化氮合酶（ＮＯＳ） 抑制剂ＬＮ６亚氨乙基赖氨酸（ＬＮＩＬ）对脓毒血症小鼠细胞能量代谢和存活率的影响。方法　制作小鼠盲肠结扎穿孔（ＣＬＰ） 动物模型,分别注射０－９ ％ 氯化钠溶液或ＬＮＩＬ或ＬＮＩＬ加Ｌ精氨酸（ＬＡｒｇ） ,比较各组小鼠肝细胞线粒体结构、心肌ＡＴＰ、ＡＤＰ含量和小鼠存活情况。结果　ＬＮＩＬ使ＣＬＰ模型小鼠肝细胞线粒体结构损伤减轻,心肌细胞内ＡＴＰ含量增加,ＡＴＰ／ＡＤＰ 比例增加,小鼠１８ 小时存活率由２０％ 增加至６０ ％ 。结论　诱导型ＮＯＳ抑制剂ＬＮＩＬ能改善脓毒血症小鼠细胞能量代谢及提高其存活率。     

白细胞介素10对大鼠肝损伤时肝星状细胞转化生长因子β1 和血小板源生长因子基因表达的影响

目的探讨白细胞介素10(IL-10)在大鼠肝损伤过程中对肝星状细胞(HSC)表达转化生长因子β1(TGFβ1)和血小板源生长因子(PDGF)的影响.方法治疗组用含有IL-10基因的腺病毒载体通过尾静脉转染大鼠(n=11),同时设立空载体组(n=12)和空白对照组(n=12),另给以皮下注射四氯化碳,每周2次,8周后处死大鼠,离体肝脏用胶原酶灌注以及密度梯度离心方法分离HSC.应用酶联免疫吸附法测大鼠血清中IL-10水平,逆转录聚合酶链反应和蛋白印迹检测HSC的TGFβ1和PDGF表达.结果治疗组的IL-10水平明显高于空载体组和空白对照组(P<0.05);治疗组HSC的TGFβ1和PDGF的mRNA、蛋白表达水平均低于空载体组和空白对照组(P<0.01).结论 IL-10可以通过下调HSC的TGFβ1和PDGF的表达来减轻肝损伤时HSC的激活程度.     

Transplantation of bone marrow-derived hepatocyte stem cells transduced with adenovirus-mediated IL-10 gene reverses liver fibrosis in rats

Bone marrow stem cells (BMSCs) transplantation alone may not be sufficient for treatment of liver fibrosis because of complicated histopathologic changes in the liver. Interleukin-10 (IL-10) is an anti-fibrosis cytokine. IL-10 gene transfer of beta2m(-)/Thy-1+ bone marrow-derived hepatocyte stem cells (BDHSCs) may be useful for treating liver fibrosis. To determine the effect of liver fibrosis in rats by transplanting BDHSCs transduced with adenovirus-mediated IL-10 gene (AdIL-10), rat BDHSCs were isolated by magnetic bead cell sorting, characterized for liver-associated phenotypes, transduced with AdIL-10, and transplanted into liver-fibrotic rats. We show that BDHSCs secreted high-level IL-10 and retained their albumin expression after AdIL-10 transfer in vitro. Intra-portal-infused BDHSCs were implanted into the liver 2 weeks after transplantation. Transplanting AdIL-10-transduced BDHSCs into liver-fibrotic rats downregulated inflammatory response, promoted liver regeneration, suppressed activation of hepatic stellate cells and improved liver histopathology and liver function. These findings demonstrated the potential utility of this novel combined strategy of IL-10 gene and BDHSCs for the treatment of liver fibrosis.     

Role of interleukin-10 in rat mesangioproliferative glomerulonephritis

SUMMARY: Interleukin-10 (IL-10) has been recognized as a growth factor for rat mesangial cells in vitro ; however, its role in mesangioproliferative glomerulonephritis is unknown. We studied the expression of IL-10 mRNA in the rat anti-Thy-1 model of mesangioproliferative glomerulonephritis (experiment 1) and, subsequently, the effects of blocking IL-10 during anti-Thy-1 nephritis using the IL-10 inhibitor, AS101 (experiment 2). In experiment 1, PCR analysis failed to detect IL-10 mRNA in normal rat kidney, however, a clear signal for IL-10 mRNA was evident on day 6 of anti-Thy-1 nephritis. In situ hybridization showed IL-10 mRNA expression in focal glomerular areas in anti-Thy-1 nephritis. Combined in situ hybridization and immunohistochemistry showed that glomerular IL-10 mRNA was expressed by both macrophages and mesangial cells. In experiment 2, treatment with AS101 significantly downregulated renal IL-10 gene expression, as demonstrated by semiquantitative PCR. However, the induction of glomerular hypercellularity, mesangial proliferation (PCNA+ cells), mesangial cell activation (α-SMA expression) and macrophage accumulation (ED1+ cells) seen in saline-treated anti-Thy-1 nephritis was unaffected by AS101 treatment. In conclusion, renal IL-10 gene expression is upregulated during pathological mesangial cell proliferation in rats with anti-Thy-1 nephritis. However, the inability of IL-10 suppression with AS101 to prevent anti-Thy-1 disease suggests that IL-10 is not essential for pathological mesangial cell proliferation.     

Prolonged survival of mouse skin allografts after transplantation of fetal liver cells transduced with hIL-10 gene

INTRODUCTION: Interleukin-10 (IL-10) is a cytokine with a moleculary weight of 18 kDa, that was first identified as being produced by Th2 cells. It appears to have anti-inflammatory action by diminishing the production of pro-inflammatory cytokines produced by Th1 cells. IL-10 also regulates the differentiation and proliferation of several immune cells such as T cells, B cells, natural killer cells, antigen-presenting cells, mast cells and granulocytes. Recent data suggest, however, that IL-10 also has immunostimulatory properties with important consequences on the prognosis of disease. In this study, we demonstrate the importance of injection of hematopoietic fetal liver cells transduced with the human IL-10 (hIL-10) gene into an allogenic recipient subsequently transplanted with allogenic skin grafts. The immaturity of stem cells and precursor cells from fetal liver and their transient survival in the host, due to the production of hIL-10, may afford 'prope' tolerance. It also explains the lack of graft-vs.-host reaction (GvHR) and the delay in rejection of the specific donor skin grafts after virtual disappearance of donor hematopoietic cells. Objectives: Transduction of CBA hematopoietic fetal cells with the human IL-10 gene was used with the aim of inducing tolerance to donor antigen in recipient BALB/c mice. The observed effects were prolonged IL-10 production, donor cell chimerism in the host and delayed rejection of skin grafts from the specific donor strain. MATERIALS AND METHODS: To prevent or delay rejection of highly incompatible skin allografts, we used IL-10 gene transfer to establish chimerism with donor hematopoietic cells. Fetal liver cells from CBA mice were transduced with the human IL-10 gene and injected into BALB/c mice. RESULTS: Human IL-10, which is active in mice but does not cross-react with murine IL-10 in ELISA, was produced in vivo for 3 weeks. Donor cells were identified in the recipients during the same time period, on the basis of presence of the H-2 k gene and human IL-10 intracellular protein. Skin allografts from CBA or C57BL/6 mice survived for a mean of 9.5 days in recipient mice injected with non-transduced cells. In contrast, survival of CBA allograft was extended to 18.9+/-1.8 days in recipients injected with hIL-10-transduced fetal liver cells from CBA mice. Human IL-10 alone, without donor hematopoietic cell engraftment, did not prolong graft survival (9.6+/-1.2 days). CONCLUSIONS: IL-10 transduction of donor hematopoietic stem cells resulted in production of IL-10, cell engraftment and chimerism. Although full tolerance was not obtained at this level of donor cell development in the host, a specific and highly significant (P<0.001) prolongation of the survival of donor skin allografts was observed.     

Effect of LAK cells on liver regeneration after partial hepatectomy

Lymphokine activated killer (LAK) cells can destroy not only tumor cells but also syngeneic regenerating liver cells. This study was started to determine the effect of passive transfer of LAK cells on liver regeneration after partial hepatectomy. C3H mice were received 70% hepatectomy and LAK cells were injected intravenously at a dose of 5 X 10(7) cells/body. After 36 hours, 3H-thymidine uptake into the residual liver was measured. LAK cells transferred group showed 31% suppression compared with control group. In vitro, 24 hours addition of LAK cells to the primary culture of regenerating liver cells caused 97% suppression of 3H-thymidine uptake at effector to target ratio, 50/1. Then we examined the effects of IL-2 administration on liver regeneration. Though IL-2 showed no effect on cultured liver cells, intraperitoneal administration of IL-2 after hepatectomy at a dose of 1 X 10(4)u/body 5 times every 8 hours brought 38% suppression of 3H-thymidine uptake of the residual liver. Cyclosporine A, which can suppress the IL-2 production of lymphocytes, promoted liver regeneration 45% over the control at a dose of 10 mg/kg. These results suggest that LAK cells could regulate liver regeneration.     

大鼠诱发肝癌模型中脾内转染IL-2和IL-12基因激活NK细胞

目的研究大鼠诱发肝癌模型中脾内直接注射携带白介素2（IL-2）和（或）白介素12（IL-12）基因的逆转录病毒包装细胞株对血IL-2和IL-12,以及NK细胞活性的影响.方法大鼠随即分为生理盐水对照组、空载体对照组、IL-12基因治疗组、IL-2基因治疗组及IL-2/IL-12联合基因治疗组.构建携带IL-2和（或）IL-12基因的逆转录病毒载体.口服二乙基亚硝胺诱癌后,含IL-2和（或）IL-12基因的包装细胞转染脾细胞.比较大鼠血IL-2和IL-12浓度、NK细胞活性、病理变化和毒性反应.结果IL基因治疗后血IL-2和IL-12明显增加.联合基因组同时表达IL-2和IL-12,总水平高于单基因治疗组.病理示治疗后肝癌组织中淋巴细胞浸润明显增多.IL治疗组NK细胞活性较对照组显著增高（P＜0.01）.联合基因组较IL单基因增高（P＜0.05）.治疗后3 d血清IL达高峰,以后逐步下降.结论脾内直接注射携带IL-2和（或）IL-12基因的逆转录包装细胞株可明显增强NK细胞活性,IL联合基因治疗优于IL单基因.     

Impaired hepatic regeneration by ischemic preconditioning in a rat model of small-for-size liver transplantation

OBJECTIVE: Graft size is one of the major risk factors in adult-to-adult living donor liver transplantation and rapid regeneration is an essential post-operative requirement. Ischemic preconditioning (IPC) has been shown to be an effective strategy in the reduction of hepatic ischemia-reperfusion injury and stimulation of liver regeneration. This study was designed to evaluate the effects of IPC on liver regeneration in small-for-size liver grafts. METHODS: We employed a rat orthotopic liver transplantation model using small-for-size (30%) grafts, in the presence or absence (control) of IPC (10 min of ischemia followed by 15 min of reperfusion). Survival rate, graft injury, hepatocellular proliferation, cell cycle progression, Stat3 activation, as well as TNF-alpha and IL-6 expression were assessed. RESULTS: IPC significantly enhanced the extent of graft injury and hindered hepatic regeneration in small-for-size liver grafts. The 7-day survival rate was also reduced by IPC, but failed to reach statistical significance. IPC did not affect TNF-alpha levels, but significantly decreased the elevation of IL-6 after reperfusion. These findings were correlated with down-regulation of cyclin E and cyclin D1, and decreased numbers of PCNA-positive nuclei in IPC grafts. These results were inconsistent with Stat3 activation, as P-Stat3 exhibited a stronger and prolonged pattern of expression in the IPC group, compared to controls. CONCLUSIONS: Ischemic preconditioning may impair liver regeneration in small-for-size liver grafts by decreasing IL-6 and blunting cell cycle progression, through a mechanism at least partially independent of Stat3.     

转染大鼠白细胞介素10基因的骨髓源性肝干细胞移植治疗大鼠肝纤维化

目的 探讨转染大鼠白细胞介素10(IL-10)基因的β2m-/Thy-1+骨髓源性肝干细胞(BDLSC)移植对大鼠肝纤维化的治疗效果.方法 分选Wistar大鼠的β3m-/Thy-1+BDLSC,转染大鼠IL-10基因.Wistar大鼠皮下注射CCl4,制作肝纤维化模型,分为3组:(1)模型组,经大鼠门静脉分支输注无菌生理盐水1 ml;(2)BDSC组,经大鼠门静脉分支输注β2m-/Thy-1+BDLSC悬液1ml(含2×105个细胞);(3)IL-10组,经大鼠门静脉分支输注转染1L-10基因的β2m-/Thy-1+BDLSC悬液1 ml(含2×105个细胞);另以皮下注射橄榄油的Wistar大鼠为对照(正常组).用细胞核染色剂二脒基苯基吲哚(DAPI)标记β2m-/Thy-1+BDLSC,以观察该细胞在肝内的定位情况.观察各组大鼠肝组织病理学改变和胶原的沉积情况,检测其肝功能和凝血功能.结果 大鼠肝组织中可见DAPI标记的β2m-/Thy-1+BDLSC.模型组大鼠的肝组织病理学改变明显,BDLSC组病理学改变有所减轻,IL-10组的组织形态最接近正常组.模型组大鼠肝组织内胶原沉积明显增多,BDLSC组胶原沉积较少,IL-10组胶原沉积明显减少.IL-10组大鼠的血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)和胆红素总量(TBIL)以及全血凝血酶原时间(PT)和活化部分凝血激酶时间(APTT)均低于模型组,差异均有统计学意义(P<0.05),其中ALT、TBIL、PT和APTT均降至正常组水平,与BDLSC组相比较,差异有统计学意义(P<0.05).结论 转染大鼠IL-10基因的β2m-/Thy-1+BDLSC移植对大鼠肝纤维化有一定的治疗效果.