中文摘要：

目的探讨人脐带间充质干细胞（hucMSC）来源的外体（exosolzleS，hucMSC—Ex）对脂多糖（LPS）诱导的人肝星状细胞系LX2活化的抑制作用及其可能机制。方法体外培养LX2细胞，分别设PBS对照组、LPS组（100ng／mL）及hucMSC—Ex组（LPS＋150μg／mLhucMSC—Ex），48h后收集细胞并提取相应的RNA及蛋白质。westernblot检测LX2活化相关指标（Ot—SMA、Collcd及TGF—J31蛋白）和凋亡指标（Bcl2、Bax及caspase3蛋白）的表达情况；lit-PCR和荧光定量RT—PCR检测d．SMAmRNA表达水平；MTT法分析hucMSC—Ex对LX2细胞活化后增殖的影响。结果LPS可刺激LX2细胞活化，活化后的LX2细胞形态由不规则形状向成纤维细胞样改变，并高表达仪-SMA、Collcd及TGF-β1蛋白，其灰度值分别上升约2．45、2．34、2．77倍（P均〈0．05）；Bax及caspase3蛋白表达下降而Bcl2蛋白表达增强；LX2增殖能力增强；经hucMSC—Ex处理后，细胞形态由细长向不规则形态转变，d—SMA、ColIod及TGF—B1蛋白表达减弱，高表达Bax及caspase3蛋白而Bcl2蛋白表达下降，且细胞增殖减少（F=23．44，P〈0．05）。结论hucMSC—Ex能够抑制LPS诱导的LX2细胞活化，降低其增殖能力并促进细胞凋亡。

英文摘要：

Objective To investigate the inhibition of exosomes derived from human umbilical cord mesenchymal stem cells （ hucMSC- Ex） on activation of human hepatic stellate cell line LX2 induced by lipopolysaceharide （LPS） and the possible mechanism. Methods LX2 cells were cultured in vitro and divided into three groups, i.e., PBS, LPS（ 100 ng/mL） and LPS plus hueMSC-Ex（ 150 μg/mL） groups. After eulyured 48 hours, the cells were collected and the cellular protein and DNA were extracted. Western blot was used to determine the levels of expressions of LX2 activation-associated proteins ： α-SMA, the specific biomarkers of LX2, as well as collagen Iαl （ColIαl） and TGF-β1. The apoptosis-associated proteins： Bel2, Bax and caspase3 were also determined. RT-PCR and quantitative RT-PCR were used to determine the level of α-SMA mRNA. The cellular viability and proliferation following activation were detected by MTT assay. Results LPS may stimulate the activation of I2（2 ceils. The shape of the cells transformed from irregular form into fibroblast-like cells. The high levels of α-SMA, colIαl and TGF-β1 protein in LX2 cells were observed in LPS-treated group, which increased 2.45, 2.34, 2.77 folds respectively （P 〈 0.05 ）, Bax and caspase3 levels decreased but Bcl2 level increased. The proliferation ability of LX2 cells enhanced. Following hucMSC-Ex treatment, the shape of the cells transformed from spindly form into irregularity and the intracellular α-SMA,colIαl and TGF-β1 decreased. The increased level of Bax and caspase3 were observed while Bcl2 level decreased, and the viability of LX2 cells reduced （ F = 23.44, P 〈 0.05）. Conclusion HucMSC-Ex could significantly inhibit the activation of LX2 induced by LPS, reduce the proliferation and promote the apoptosis of LX2 cells induced by LPS.