Ono M, Kohda H, Kawaguchi T, Ohhira M, Sekiya C, Namiki M, Takeyasu A, Taniguchi N
Department of Internal Medicine III, Asahikawa Medical College, Hokkaido, Japan.
Biochem Biophys Res Commun. 1992 Feb 14;182(3):1100-7. doi: 10.1016/0006-291x(92)91845-h.
Effects of Tumor Necrosis Factor (TNF), Interleukin-1 (IL-1), Interleukin-6 (IL-6) and Interferon-gamma (IFN-gamma) on the expression of Mn-superoxide dismutase (Mn-SOD) protein were investigated in human hepatoma cells, Hu-H1, which revealed resistance to the cytotoxicity of TNF and IL-1. Both TNF and IL-1 enhanced the Mn-SOD production to the level of 30- to 40-fold. IL-6 also increased the enzyme protein to 2- to 3-fold of the basal level without any cell proliferative effect. A specific antibody against IL-6 almost completely inhibited the induction of Mn-SOD. IL-6, as well as TNF and IL-1, appears to play some role in the Mn-SOD protein expression in human hepatoma cells.
在对肿瘤坏死因子（TNF）、白细胞介素-1（IL-1）、白细胞介素-6（IL-6）和干扰素-γ（IFN-γ）对人肝癌细胞Hu-H1中锰超氧化物歧化酶（Mn-SOD）蛋白表达的影响进行研究时发现，该细胞对TNF和IL-1的细胞毒性具有抗性。TNF和IL-1均将Mn-SOD的产生增强至30至40倍的水平。IL-6也使该酶蛋白增加至基础水平的2至3倍，且无任何细胞增殖作用。一种针对IL-6的特异性抗体几乎完全抑制了Mn-SOD的诱导。IL-6以及TNF和IL-1似乎在人肝癌细胞的Mn-SOD蛋白表达中发挥了一定作用。
