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目的:探讨小鼠脂肪间充质干细胞(ADSCs)能否减缓百草枯中毒引起的小鼠肺损伤。方法:体外分离和培养小鼠ADSCs并观察细胞形态;取第3代细胞,采用流式细胞仪检测细胞表面标志物CD29、CD31、CD34、CD90和CD105的表达情况;另取第3代细胞,进行成脂和成骨诱导分化鉴定。45只SPF级雄性C57BL/6小鼠随机分为3组:百草枯组、ADSCs治疗组以及正常对照组。通过尾静脉注射ADSCs到小鼠体内,观察小鼠血浆中肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)的表达变化和肺组织纤维化程度的变化。结果:分离培养的细胞呈典型的成纤维样;细胞CD29、CD90、CD105阳性表达率分别高达99.5%,94.8%,73.7%;CD31和CD34阳性表达率几乎为0;细胞经诱导后可分化为脂肪细胞和成骨细胞。综上,细胞鉴定为ADSCs。与百草枯组比较,ADSCs治疗组可明显降低血浆中TNF-α、IL-1β的含量(P<0.05);肺组织Masson染色显示ADSCs治疗组能够降低肺组织纤维化程度。结论:ADSCs可减缓急性百草枯中毒引起的肺损伤。
Objective: To investigate whether ADSCs can attenuate lung injury in mice induced by paraquat poisoning. Methods: The ADSCs of mice were isolated and cultured in vitro and the morphology of the cells was observed. The third generation cells were used to detect the expression of cell surface markers CD29, CD31, CD34, CD90 and CD105 by flow cytometry. To adipogenic and osteogenic differentiation identification. Forty-five SPF male C57BL / 6 mice were randomly divided into three groups: paraquat group, ADSCs group and normal control group. ADSCs were injected into the tail vein of mice to observe the changes of the expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and the degree of lung fibrosis in mice. Results: The isolated and cultured cells showed typical fibroblast-like morphology. The positive rates of CD29, CD90 and CD105 were 99.5%, 94.8% and 73.7%, respectively. The positive rates of CD31 and CD34 were almost zero. Adipocytes and osteoblasts. In summary, the cells were identified as ADSCs. Compared with the paraquat group, ADSCs treatment group can significantly reduce the plasma levels of TNF-α, IL-1β (P <0.05); Masson staining of lung tissue showed ADSCs treatment group can reduce the degree of lung fibrosis. Conclusion: ADSCs can slow the lung injury caused by acute paraquat poisoning.