【摘要】：目的:研究骨髓間充質(zhì)干細(xì)胞(BMSCs)在肝細(xì)胞損傷恢復(fù)中的作用,并探討可能機(jī)制。方法:(1)培養(yǎng)原代肝細(xì)胞及BMSCs并鑒定;(2)建立損傷肝細(xì)胞模型;(3)MTT法檢測(cè)不同條件下肝細(xì)胞增殖情況;(4)加入BMSCs、bax抑制劑、BMSCs+bax抑制劑進(jìn)行共培養(yǎng),采用Western-blot和real-time PCR法檢測(cè)TGF-β1、bcl-2、bax等指標(biāo)。結(jié)果:(1)BMSCs+HGF共培養(yǎng)組中的OD值明顯高于BMSCs或HGF單獨(dú)聯(lián)合培養(yǎng)組(P0.05),BMSCs與HGF單獨(dú)共培養(yǎng)組之間OD值差異無統(tǒng)計(jì)學(xué)意義,而它們與對(duì)照組相比差異均有統(tǒng)計(jì)學(xué)意義(P0.05)。(2)bax1抑制劑共培養(yǎng)組與BMSCs共培養(yǎng)組的OD值差異無統(tǒng)計(jì)學(xué)意義,兩者與對(duì)照組相比差異有統(tǒng)計(jì)學(xué)意義(P0.05),BMSCs+Bax-1共培養(yǎng)組的OD值與BMSCs或bax1共培養(yǎng)組差異無統(tǒng)計(jì)學(xué)意義。(3)Western-blot法及real-time PCR檢測(cè)結(jié)果提示TGF-β1、bax在bax1抑制劑共培養(yǎng)組與BMSCs共培養(yǎng)組中均顯著低于對(duì)照組(P0.05),而BMSCs+Bax-1抑制劑共培養(yǎng)組與兩者單獨(dú)共培養(yǎng)差異無統(tǒng)計(jì)學(xué)意義,Bcl-2結(jié)果與前兩者相反。結(jié)論:BMSCs在肝細(xì)胞損傷恢復(fù)中能促進(jìn)肝細(xì)胞增殖,BMSCs促進(jìn)肝細(xì)胞增殖通過調(diào)節(jié)TGF-β1/bcl-2(bax)這個(gè)信號(hào)通道減少凋亡來實(shí)現(xiàn)的。
[Abstract]:Aim: to study the role of bone marrow mesenchymal stem cell (BMSCs) in the recovery of hepatocyte injury and explore the possible mechanism. Methods: (1) primary hepatocytes and BMSCs were cultured and identified; (2) hepatocyte injury model was established; (3) MTT method was used to detect the proliferation of hepatocytes under different conditions. (4) BMSCs,bax inhibitor, BMSCs bax inhibitor was added to co-culture, Western-blot and real-time PCR methods were used to detect TGF- 尾 1 bcl-2bax and so on. Results: (1) the OD value in) BMSCs HGF co-culture group was significantly higher than that in BMSCs or HGF co-culture group (P0.05). There was no significant difference in OD value between), BMSCs and HGF co-culture group. There was no significant difference in OD between bax1 inhibitor co-culture group and BMSCs co-culture group (P0.05), but there was significant difference between them compared with control group (P0.05). The OD value of BMSCs Bax-1 coculture group was not significantly different from that of BMSCs or bax1 co-culture group. (3) the results of Western-blot and real-time PCR showed that TGF- 尾 _ 1 was not significantly different from that of BMSCs or bax1 co-culture group. Bax was significantly lower in bax1 inhibitor co-culture group and BMSCs co-culture group than in control group (P0.05), but there was no significant difference between BMSCs Bax-1 inhibitor co-culture group and BMSCs Bax-1 inhibitor co-culture group. Bcl-2 results were contrary to the former two groups. Conclusion: BMSCs can promote the proliferation of hepatocytes during the recovery of hepatocyte injury, and BMSCs can promote the proliferation of hepatocytes by regulating the signal channel of TGF- 尾 1/bcl-2 (bax) to reduce apoptosis.
【作者單位】： 解放軍第16醫(yī)院普外科;解放軍第16醫(yī)院醫(yī)務(wù)處;第三軍醫(yī)大學(xué)西南醫(yī)院全軍肝膽外科研究所;
【基金】：全軍醫(yī)學(xué)科技青年培育項(xiàng)目(編號(hào):13QNP023)
【分類號(hào)】：R657.3

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