The protective effect of adipose-derived stem cells against liver injury by trophic molecules

被引:23
作者
Saito, Yu [1 ]
Shimada, Mitsuo [1 ]
Utsunomiya, Tohru [1 ]
Ikemoto, Tetsuya [1 ]
Yamada, Shinichiro [1 ]
Morine, Yuji [1 ]
Imura, Satoru [1 ]
Mori, Hiroki [1 ]
Sugimoto, Koji [1 ]
Iwahashi, Shuichi [1 ]
Asanoma, Michihito [1 ]
机构
[1] Univ Tokushima, Dept Surg, Inst Hlth Biosci, Grad Sch, Tokushima 7708503, Japan
关键词
Adipose-derived stem cells; Hepatocytes; Vascular endothelial growth factor; ENDOTHELIAL GROWTH-FACTOR; IN-VIVO; EPITHELIAL-CELLS; RAT-LIVER; TISSUE; TRANSPLANTATION; HEPATECTOMY; ISLETS; MICE; ANGIOGENESIS;
D O I
10.1016/j.jss.2012.10.009
中图分类号
R61 [外科手术学];
学科分类号
摘要
Background: In this study we investigated whether adipose-derived stem cells (ADSCs) had any beneficial protective effects on liver injury and regeneration in vivo. Moreover, we examined whether ADSCs protect hepatocytes via trophic molecules. Materials and methods: We transplanted ADSCs into mice after 70% hepatectomy and ischemia-reperfusion, and observed liver injury and regeneration after reperfusion. We co-cultured hepatocytes with ADSCs using a Transwell system for 7 d and evaluated the viabilities of hepatocytes and the cytokine levels in the culture medium. Bevacizumab was used to confirm the effect of vascular endothelial growth factor (VEGF) on hepatocytes. Results: ADSCs improved serum liver function at 6 h after reperfusion in a nonlethal model and stimulated liver regeneration at 24 h after reperfusion in a lethal model. VEGF levels in the culture medium were increased by co-culture ADSCs with hepatocytes. ADSCs improved the viabilities of hepatocytes. The inhibited production of VEGF by bevacizumab did not affect the viability of hepatocytes. Conclusions: ADSCs were able to ameliorate liver injury and stimulate liver regeneration in subsequent hepatectomy and ischemia-reperfusion-injured model mice. Furthermore, hepatocytes were protected by the trophic molecules of the ADSCs. However, such protective effects might be provided by mechanisms other than VEGF signaling. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:162 / 168
页数:7
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