Sato K, Kasono K, Fujii Y, Kawakami M, Tsushima T, Shizume K
Biochem Biophys Res Commun. 1987 May 29;145(1):323-9. doi: 10.1016/0006-291x(87)91324-6.
To elucidate the mechanism of tumor necrosis factor alpha (TNF-alpha)-induced bone resorption, the effects of recombinant human TNF-alpha on mouse osteoblast-like cells (MC3T3-E1) were studied. TNF-alpha stimulated MC3T3-E1 cells to produce prostaglandin E2 (PGE2) and macrophage colony stimulating activity (M-CSA) in a dose-dependent manner. TNF decreased alkaline phosphatase (AL-P) activity of MC3T3-E1 cells. These TNF effects were observed at 1 ng/ml (approximately 6 X 10(-11)M). The inhibitory effect on AL-P activity was reversible and the cell growth of MC3T3-E1 cells was only slightly affected by TNF. These findings suggest that both PGE2 and M-CSA stimulated by TNF-alpha are possibly involved in osteoblast-mediated osteoclastic bone resorption, whereas inhibition of AL-P activity may lead to a decrease in bone formation.
为阐明肿瘤坏死因子α（TNF-α）诱导骨吸收的机制，研究了重组人TNF-α对小鼠成骨样细胞（MC3T3-E1）的影响。TNF-α以剂量依赖性方式刺激MC3T3-E1细胞产生前列腺素E2（PGE2）和巨噬细胞集落刺激活性（M-CSA）。TNF降低了MC3T3-E1细胞的碱性磷酸酶（AL-P）活性。在1 ng/ml（约6×10^(-11)M）时观察到这些TNF效应。对AL-P活性的抑制作用是可逆的，且TNF对MC3T3-E1细胞的生长仅有轻微影响。这些发现表明，TNF-α刺激产生的PGE2和M-CSA可能都参与了成骨细胞介导的破骨细胞骨吸收，而AL-P活性的抑制可能导致骨形成减少。
