Lertchirakarn V, Birner R, Messer H H
School of Dental Science, University of Melbourne, Victoria, Australia.
J Endod. 1998 Jun;24(6):409-13. doi: 10.1016/S0099-2399(98)80022-8.
The aim of this study was to investigate the effect of interleukin-1 beta (IL-1 beta) on pulpal fibroblast proliferation and collagen synthesis in vitro. Cell proliferation was assessed by [3H]thymidine uptake at 24, 48, and 72 h. These cells were compared with dermal fibroblasts under a range of conditions. IL-1 beta inhibited pulp cell proliferation, but this effect was decreased by the presence of indomethacin. In contrast, IL-1 beta stimulated dermal fibroblast proliferation in the absence and presence of indomethacin. Collagen synthesis was analyzed by incorporation of 5-[3H]proline into polypeptide chains. IL-1 beta stimulated synthesis of type I collagen both in the absence and presence of indomethacin. Results suggest that the inhibitory effect on pulp cell proliferation is dependent upon IL-1 beta-induced prostaglandin E2 synthesis and that IL-1 beta is a potent mediator of prostaglandin E2 synthesis in dental pulp. These observations imply a role of IL-1 beta in collagen synthesis, but not in the fibroblast proliferation phase of the healing process.
本研究的目的是在体外研究白细胞介素-1β(IL-1β)对牙髓成纤维细胞增殖和胶原合成的影响。通过在24、48和72小时时检测[3H]胸腺嘧啶核苷摄取来评估细胞增殖。在一系列条件下将这些细胞与皮肤成纤维细胞进行比较。IL-1β抑制牙髓细胞增殖,但吲哚美辛的存在可减弱这种作用。相反,在不存在和存在吲哚美辛的情况下,IL-1β均刺激皮肤成纤维细胞增殖。通过将5-[3H]脯氨酸掺入多肽链来分析胶原合成。在不存在和存在吲哚美辛的情况下,IL-1β均刺激I型胶原的合成。结果表明,对牙髓细胞增殖的抑制作用取决于IL-1β诱导的前列腺素E2合成,并且IL-1β是牙髓中前列腺素E2合成的有效介质。这些观察结果表明IL-1β在胶原合成中起作用,但在愈合过程的成纤维细胞增殖阶段不起作用。