中文摘要：

目的 采用脂多糖（LPS）诱导大鼠枯否细胞（KCs）发生极化改变,之后用人脐带血间充质干细胞（huMSCs）与LPS诱导的KCs在Transwell内共培养,以观察huMSCs对KCs极化偏移的调节作用。方法 实验分为KCs组、KCs＋LPS组、MSCs＋KCs＋LPS组。对各组的白介素-4（IL-4）、肿瘤坏死因子（TNF-α）、白介素-10（IL-10）、白介素-6（IL-6）等上清因子采用ELISA法进行检测;诱导型一氧化氮合酶（iN-OS）、精氨酸酶-1（Arg-1）、信号传导与转录激活因子3、6（STAT-3、STAT-6）、核因子kappaB（NF-κB）用Westernbolt进行检测,同时用荧光实时定量PCR（qRT-PCR）对以上结果进行验证。结果 KCs＋LPS组促炎因子TNF-α、IL-6分泌增加,MSCs＋KCs＋LPS组抑炎因子IL-10、IL-4分泌增加;而Westernblot检测表明,KCs＋LPS组中iNOS升高,NF-κB p65入核增高;而MSCs＋KCs＋LPS组高表达Arg-1,同时pSTAT-3、pSTAT-6表达增加。结论 huMSCs能诱导已经发生M1极化的KCs向M2表型偏移,考虑可能与huMSCs分泌细胞因子有关,起到一种免疫调节作用,huMSCs调节巨噬细胞极化的分子机制可能与通过JAK-STAT信号转导通路有关。

英文摘要：

Objective LPS-stimulated Kupffer cells （KCs） cells （buMSCs） were co-cultured in Transwell to observe the and human umbilical cord blood mesenchymal stem effect of huMSCs on the polarization of KCs. Methods During this study, the model of huMSCs in vitro co-culturing with KCs was built, and three groups were as- signed, which were KCs group（ normal group）, KCs cells ＋ LPS group（ control group）, KCs ＋ LPS ＋ MSCs group （experimental group）. Among the three groups, IL-4, TNF-α, IL-10, IL-6 were detected by ELISA while induc- ible nitricoxide synthase （iNOS）, arginase-1 （Arg-1）, phosphorylation reaction level of signal transducer and acti- vator of transcription-3,6 （STAT-3, STAT-6） and nuclear factor-KB （NF-KB） were detected by Western bolt. After that, qRT-PCT was adopted to check the previous results. Results It was found that both TNF-α and IL-6 secre- tion increased in the control group, while both IL-10 and IL-4 secretion increased in the experimental group. West- ern blot detection showed that the level of iNOS increased in the control group, NF-KB p65 increased in the nucle- us, while the experimental group was high expression of Arg-1, pSTAT-6, pSTAT-3. Conclusion Our experi- ment＇ s findings indicate that huMSCs can induce alternative activation of KCs, and the activation pathway might be the JAK-STAT pathways.