Chen W, Steffan A M, Braunwald J, Nonnenmacher H, Kirn A, Gendrault J L
Laboratoire de Virologie, Faculté de Médecine Unité de Recherches INSERM U743, Strasbourg, France.
J Hepatol. 1990 Nov;11(3):330-8. doi: 10.1016/0168-8278(90)90217-f.
In this study we demonstrate that hepatocytes isolated from normal mice may efficiently inhibit the multiplication of fat-storing cells (FSC) in culture, either in a coculture system where both cell types are separated by a filter of 0.45 microns pore size or via their conditioned medium. The inhibition may be completely reversed when the hepatocytes are removed and the culture medium is renewed. The inhibitory factor appears as early as 8 h in the medium with an almost maximum effect being reached after 24 h, as long as protein synthesis is allowed. It rapidly loses its efficiency through dilution. The inhibitory capacity of the conditioned medium is maintained after heating at 56 degrees C, dialysis of 100,000 x g centrifugation, but reduced after trypsin treatment. The infection of the hepatocytes by ectromelia virus causes an almost total suppression of the synthesis of the inhibitory factor. This latter result suggests that the multiplication of FSC, which may be inhibited by normal hepatocytes, would no longer be hindered in case of disregulation.
在本研究中，我们证明从正常小鼠分离的肝细胞可有效抑制培养中的贮脂细胞（FSC）增殖，无论是在两种细胞类型由孔径为0.45微米的滤膜分隔的共培养系统中，还是通过其条件培养基。当去除肝细胞并更换培养基时，抑制作用可能完全逆转。只要允许蛋白质合成，抑制因子最早在培养基中8小时出现，24小时后达到几乎最大效果。它通过稀释迅速失去其效力。条件培养基在56℃加热、100,000×g离心透析后仍保持抑制能力，但胰蛋白酶处理后降低。埃可病毒感染肝细胞几乎完全抑制了抑制因子的合成。后一结果表明，正常肝细胞可能抑制的FSC增殖在失调情况下将不再受到阻碍。
