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目的探讨丙烯醇导致的肝损伤环境对大鼠骨髓来源的Thy-1+β2M-细胞(BDTCs)向肝脏细胞诱导分化的影响。方法用免疫磁分选方法分离雄性F344大鼠BDTCs,以PKH26标记后经门静脉输注入受者雌性F344大鼠体内。30只受者随机分为3组,A组:丙烯醇损伤+BDTCs移植组;B组:正常+BDTCs移植组;C组:丙烯醇损伤+等渗盐水对照组。术后不同时间行血清生物化学检测,经荧光标记细胞定位、原位杂交检测Y染色体sry基因表达和免疫组织化学等方法检测移植的BDTCs在受体肝脏内分布、增殖和分化情况。结果荧光显微镜和sry基因原位杂交均发现,供体BDTCs在丙烯醇所致的坏死汇管区附近呈片状或索条状分布;免疫组织化学结果显示,汇管区附近的部分新生细胞序贯性表达OV-6、甲胎蛋白、细胞角蛋白19和白蛋白,而B组肝内几乎未见阳性细胞出现;A组和C组血清生物化学指标恢复正常所需时间分别为(9.8±3.1)d和(13.7±4.2)d。结论丙烯醇致肝汇管区坏死的微环境有利于BDTCs整合至肝细胞板中并向成熟的肝细胞分化,BDTCs在向肝细胞分化的同时还可能促进内源性的肝细胞再生和修复。
Objective To investigate the effects of enol-induced liver injury on the differentiation of rat bone marrow-derived Thy-1 + β2M-cells (BDTCs) into hepatocytes. Methods The male F344 rats BDTCs were isolated by immunomagnetic separation method and were injected with PKH26 into the recipient female F344 rats via portal vein. 30 recipients were randomly divided into 3 groups: group A: propylene glycol injury + BDTCs transplantation group; group B: normal + BDTCs transplantation group; group C: propylene alcohol injury + isotonic saline control group. Serum biochemical tests were performed at different times after operation. The distribution, proliferation and differentiation of transplanted BDTCs in the recipient liver were detected by fluorescence labeled cells localization, in situ hybridization detection of Y chromosome sry gene expression and immunohistochemistry. Results Fluorescent microscopy and sry gene in situ hybridization found that BDTCs donated in the vicinity of the necrotic portal area caused by allyl alcohol were lamellar or cord-like distribution; immunohistochemical results showed that part of the neonatal cells near the portal area of the sequential The expression of OV-6, alpha-fetoprotein, cytokeratin 19, and albumin were not observed in the liver of group B, and the serum biochemical parameters of group A and group C returned to normal (9.8 ± 3.1) d and (13.7 ± 4.2) d. CONCLUSION: The microenvironment of alveolar epithelial cell necrosis induced by allyl alcohol facilitates the integration of BDTCs into hepatocytes and the differentiation into mature hepatocytes. BDTCs may also promote the regeneration and repair of endogenous hepatocytes while differentiating into hepatocytes.