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聚电解质复合物(PEC)对人牙周膜成纤维细胞(HPLF)功能的影响。II. L-抗坏血酸和地塞米松对HPLF在PEC上分化和聚集的增强作用。

Effects of polyelectrolyte complex (PEC) on human periodontal ligament fibroblast (HPLF) function. II. Enhancement of HPLF differentiation and aggregation on PEC by L-ascorbic acid and dexamethasone.

作者信息

Hamano T, Teramoto A, Iizuka E, Abe K

机构信息

Department of Functional Polymer Science, Faculty of Textile Science and Technology, Shinshu University, Ueda, Japan.

出版信息

J Biomed Mater Res. 1998 Aug;41(2):270-7. doi: 10.1002/(sici)1097-4636(199808)41:2<270::aid-jbm12>3.0.co;2-p.

Abstract

In addition to many types of extra cellular matrix (ECM) in vivo, cells are stimulated by many types of vitamins, hormones, growth factors, etc. In this paper the effects of L-ascorbic acid 2-phosphate (Asc-2P) and dexamethasone (Dex) on proliferation and differentiation of human periodontal ligament fibroblast (HPLF) using polyelectrolyte complex (PEC) as a matrix in vitro will be discussed. The PEC was composed of chitosan as a polycation, with carboxymethyl (CPEC) or sulfated chitin (SPEC). Asc-2P (0.2 mM) inhibited the growth of HPLF on CPEC, but promoted the growth on SPEC. Moreover, the aggregation of HPLF on CPEC was inhibited by Asc-2P, but that on SPEC was induced in the presence of Asc-2P and Dex. Although Asc-2P reduced an increase in alkaline phosphatase (ALPase) activity of HPLF on CPEC as well, it induced a twofold increase in ALPase activities on SPEC and TCD. Furthermore, in the medium containing Asc-2P and 100 mM of Dex, cell growth was inhibited, but ALPase activity was promoted on both SPEC and TCD to form many aggregates on SPEC. ALPase activity increased by twofold over that of HPLF cultured in the medium containing only Asc-2P. Therefore, it is suggested that the cell functions of HPLF are controlled by the combination of PEC and additives.

摘要

除了体内多种类型的细胞外基质(ECM),细胞还受到多种维生素、激素、生长因子等的刺激。本文将讨论以聚电解质复合物(PEC)为基质,在体外研究L-抗坏血酸2-磷酸酯(Asc-2P)和地塞米松(Dex)对人牙周膜成纤维细胞(HPLF)增殖和分化的影响。PEC由壳聚糖作为聚阳离子与羧甲基壳聚糖(CPEC)或硫酸化甲壳素(SPEC)组成。Asc-2P(0.2 mM)抑制HPLF在CPEC上的生长,但促进其在SPEC上的生长。此外,Asc-2P抑制HPLF在CPEC上的聚集,但在Asc-2P和Dex存在的情况下诱导其在SPEC上的聚集。虽然Asc-2P也降低了HPLF在CPEC上碱性磷酸酶(ALPase)活性的增加,但它在SPEC和TCD上诱导ALPase活性增加了两倍。此外,在含有Asc-2P和100 mM Dex的培养基中,细胞生长受到抑制,但在SPEC和TCD上ALPase活性均得到促进,在SPEC上形成许多聚集体。ALPase活性比仅在含有Asc-2P的培养基中培养的HPLF增加了两倍。因此,提示HPLF的细胞功能受PEC和添加剂组合的调控。

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