Cytotoxicity of chlorhexidine on human osteoblastic cells is related to intracellular glutathione levels

被引:58
|
作者
Lee, T. -H. [1 ,2 ]
Hu, C. -C. [3 ]
Lee, S. -S. [4 ]
Chou, M. -Y. [5 ]
Chang, Y. -C. [2 ,5 ]
机构
[1] Chung Shan Med Univ, Inst Med, Taichung, Taiwan
[2] Chung Shan Med Univ Hosp, Dept Dent, Taichung, Taiwan
[3] Chung Shan Med Univ, Sch Appl Chem, Taichung, Taiwan
[4] Chung Shan Med Univ, Sch Publ Hlth, Taichung, Taiwan
[5] Chung Shan Med Univ, Sch Dent, Taichung, Taiwan
关键词
chlorhexidine; cytotoxicity; glutathione; osteoblastic cells; FIBROBLASTS IN-VITRO; CALCIUM HYDROXIDE; ENTEROCOCCUS-FAECALIS; GLUCONATE; MECHANISMS; THERAPY; IODINE;
D O I
10.1111/j.1365-2591.2010.01700.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
P>Aim To evaluate the mechanisms of cytotoxicity of chlorhexidine (CHX) in human osteoblastic cells in vitro. Methodology Cytotoxicity, cell proliferation and collagen synthesis assays were performed to elucidate the toxic effects of CHX on the human osteoblastic cell line U2OS. To determine whether glutathione (GSH) levels were important in the cytotoxicity of CHX, cells were pre-treated with 2-oxothiazolidine-4-carboxylic acid (OTZ) to boost GSH levels or buthionine sulfoximine (BSO) to deplete GSH. Results CHX demonstrated a cytotoxic effect to U2OS cells in a dose-dependent manner (P < 0.05). The 50% inhibition concentration of CHX was approximately 0.005%. CHX also inhibited cell proliferation and collagen synthesis (P < 0.05). The addition of OTZ acted as a protective effect on the CHX-induced cytotoxicity (P < 0.05). In contrast, the addition of BSO enhanced the CHX-induced cytotoxicity (P < 0.05). Conclusions The levels of CHX tested inhibited cell growth, proliferation and collagen synthesis on U2OS cells. CHX has significant potential for periapical toxicity. GSH depletion might be one of the mechanisms underlying CHX cytotoxicity.
引用
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页码:430 / 435
页数:6
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