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Th17细胞在胰岛移植中的作用 总被引:1,自引:0,他引:1
目的 研究Th17细胞在胰岛移植免疫排斥反应中的作用,探讨IL-23R抗体联合应用Anti-CD154mAb诱导胰岛移植免疫耐受的可行性.方法 体外实验分为5组:空白对照组,SD大鼠胰岛细胞单独培养;A组,大鼠胰岛细胞混合淋巴细胞培养,不加IL-23R抗体;B、C、D组,将大鼠胰岛细胞混合淋巴细胞培养,分别加IL-23R抗体0.1 μg/mL、0.5 μg/mL、1.0 μg/mL.作细胞甩片后,行丫啶橙(AO)/碘化丙啶(PI)荧光染色、胰岛素和胰高血糖索免疫组化染色、胰岛素刺激实验.体内实验(将分离纯化的胰岛移植于小鼠左肾包膜下)分成4组:对照组,胰岛移植后不予任何干预;IL-23R抗体(200 μg)治疗组;Anti-CD154mAb(200 μg)治疗组;联合治疗组.监测移植后小鼠血糖,取移植肾作HE染色及胰岛素、胰高血糖素免疫组化染色.结果 共培养3 d后,在胰岛素刺激实验中,空白对照组的葡萄糖刺激指数为3.66±0.10,与A、B、C、D组相比升高(P<0.05).D组刺激指数高于其他各组,达到1.95±0.75.胰岛素和胰高血糖素免疫组化染色,体外和体内实验显示各实验组移植物有功能存活明显好于对照组.移植3 d后,对照组血糖与各实验组相比升高(P<0.05),各实验组血糖比较无明显差异.结论 Th17细胞参与了胰岛移植的免疫排斥反应.通过阻断IL-23R能有效的下调IL-17的表达,阻断效果呈剂量依赖性.Anti-CDl54mAb和IL-23R抗体联合应用能在一定程度上防止胰岛移植物的急性排斥反应,但与单独使用Anti-CD154mAb治疗相比无明显差异. 相似文献
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经后上腰腹膜后引流及灌洗治疗胰腺感染性坏死(附45例报告) 总被引:1,自引:0,他引:1
胰腺及胰周坏死组织继发感染是急性胰腺炎(AP)的严重并发症,也是导致其高死亡率的原因.目前,国内外学者一致认为AP继发胰腺感染性坏死(IN)的手术治疗是必要的,但术式并不统一[1-3].我院采用经后上腰腹膜后引流术及术后灌洗治疗胰腺感染性坏死45例,取得较满意疗效,报道如下. 相似文献
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BACKGROUND: Bone marrow mesenchymal stem cells are likely to repair renal injury by differentiating into renal parenchymal cells.
OBJECTIVE: To explore the effect and mechanism of bone marrow mesenchymal stem cells in the renal repair after mesangial proliferative glomerulonephritis.
METHODS: Thirty Sprague-Dawley rats were randomized into normal group, model group and treatment group (n=10 per group). Model group and treatment group were treated with tail vein injection of mouse anti-rat monoclonal antibody Thy1.1 to prepare mesangial proliferative glomerulonephritis models. One week after modeling, rats in the treatment group were given 2×106 bone marrow mesenchymal stem cells via the tail vein, and rats in the other two groups were given the same volume of normal saline. Two weeks after transplantation, urinary protein, urea nitrogen, creatinine levels were detected; hematoxylin-eosin staining was used for observing pathological changes of the renal tissue under microscope; and the expression of transforming growth factor beta 1 was detected by immunohistochemistry method.
RESULTS AND CONCLUSION: The levels of urinary protein, urea nitrogen and creatinine as well as the expression of transforming growth factor beta 1 in the renal tissue arranged in descending order were listed as follows: model group > treatment group > control group, and there were significant differences among three groups (P < 0.05). In the model group, diffuse glomerular hyperplasia was observed with the presence of increased extracellular matrix, partial glomerular sclerosis, and interstitial infiltration of inflammatory cells; in the treatment group, glomerular hyperplasia, mesangial proliferation and inflammatory cell infiltration were all mitigated compared with the model group. Therefore, bone marrow mesenchymal stem cell transplantation may contribute to renal repair after mesangial proliferative glomerulonephritis, by inhibiting overexpression of transforming growth factor beta 1 in the kidney.
中国组织工程研究杂志出版内容重点:干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程 相似文献
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病例资料患者,女,59岁,因"皮肤、巩膜黄染进行性加重3个月"入院。入院前3个月患者无明显诱因出现皮肤、巩膜黄染,症状进行性加重,不伴腹痛、寒战、高热等症状。在外院行核磁共振成像提示"肝门胆管阻塞,考虑肝门胆管癌",遂来我院进一步诊治,门诊以"梗阻性黄疸"收入我院肝胆胰外科。患者既往身体良好,否认肝炎、结核或其他传染病史,否认长期药物及工业毒物接触史。入院查体:皮肤、 相似文献
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