Laboratory of Pharmacology, Toxicology & Pulp Biology, Department of Dentistry and School of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan.
Int Endod J. 2012 Sep;45(9):848-58. doi: 10.1111/j.1365-2591.2012.02042.x. Epub 2012 Apr 6.
To evaluate the effect of TEGDMA on cell cycle progression as well as alterations of cell cycle-related gene and protein expression.
Human dental pulp cells were exposed to 0-5 mmol L(-1) TEGDMA for 24 h. Cytotoxicity was evaluated by 3-(4, 5-dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. Cell cycle progression was analysed by propidium iodide (PI) flow cytometry. Cell death pathway was surveyed by annexin V/PI dual-staining flow cytometry. The mRNA expression of cell cycle-related genes (cdc2, cyclinB1 and p21) and COX-2 was evaluated by reverse transcriptase-polymerase chain reaction, and their protein expression was evaluated by Western blotting. The production of PGE(2) and PGF(2α) in the culture medium was determined by enzyme-linked immunosorbent assay.
Triethylene glycol dimethacrylate inhibited cellular growth and induced cell cycle deregulation in dental pulp cells. High-dose exposure provoked both necrotic and apoptotic cell death. The gene and protein expression of cdc2, cyclin B1 and cdc25C declined obviously whilst cells treated with 2.5 mmol L(-1) TEGDMA concurrent with the elevated expression of p21. The mRNA and protein expression of COX-2, along with production of PGE(2) and PGF(2α), are drastically raised by 2.5-5 mmol L(-1) TEGDMA.
Triethylene glycol dimethacrylate induced cytotoxicity, cell cycle arrest and apoptosis in dental pulp cells, which was associated with the decline of cdc2, cyclin B1, cdc25C expression and elevation of p21 expression. Concomitantly, COX-2 expression, PGE(2) and PGF(2α) production increased. These effects may contribute to explain the pulpal damage and inflammation induced by TEGDMA after operative procedures.
评估三乙二醇二甲基丙烯酸酯（TEGDMA）对细胞周期进程的影响，以及细胞周期相关基因和蛋白表达的改变。
将人牙髓细胞暴露于 0-5mmol/L TEGDMA 中 24 小时。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐（MTT）比色法评估细胞毒性。通过碘化丙啶（PI）流式细胞术分析细胞周期进程。通过 Annexin V/PI 双染流式细胞术检测细胞死亡途径。通过逆转录-聚合酶链反应（RT-PCR）评估细胞周期相关基因（cdc2、cyclinB1 和 p21）和 COX-2 的 mRNA 表达，通过 Western blot 评估其蛋白表达。通过酶联免疫吸附试验（ELISA）测定培养基中 PGE（2）和 PGF（2α）的产生。
三乙二醇二甲基丙烯酸酯抑制牙髓细胞的细胞生长并诱导细胞周期失调。高剂量暴露引起坏死和凋亡细胞死亡。用 2.5mmol/L TEGDMA 处理后，cdc2、cyclin B1 和 cdc25C 的基因和蛋白表达明显下降，同时 p21 表达升高。2.5-5mmol/L TEGDMA 可显著上调 COX-2 的 mRNA 和蛋白表达，以及 PGE（2）和 PGF（2α）的产生。
三乙二醇二甲基丙烯酸酯诱导牙髓细胞产生细胞毒性、细胞周期停滞和凋亡，这与 cdc2、cyclin B1、cdc25C 表达下降和 p21 表达升高有关。同时，COX-2 表达、PGE（2）和 PGF（2α）的产生增加。这些影响可能有助于解释手术操作后 TEGDMA 引起的牙髓损伤和炎症。
