Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Int Endod J. 2010 May;43(5):430-5. doi: 10.1111/j.1365-2591.2010.01700.x.
To evaluate the mechanisms of cytotoxicity of chlorhexidine (CHX) in human osteoblastic cells in vitro.
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.
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).
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.
评估体外人成骨细胞中洗必泰（CHX）细胞毒性的机制。
采用细胞毒性、细胞增殖和胶原合成检测方法，阐明 CHX 对人成骨细胞系 U2OS 的毒性作用。为了确定谷胱甘肽（GSH）水平是否对 CHX 的细胞毒性很重要，用 2-氧代噻唑烷-4-羧酸（OTZ）预处理细胞以提高 GSH 水平，或用丁硫氨酸亚砜（BSO）耗尽 GSH。
CHX 对 U2OS 细胞呈剂量依赖性细胞毒性作用（P<0.05）。CHX 的 50%抑制浓度约为 0.005%。CHX 还抑制细胞增殖和胶原合成（P<0.05）。OTZ 的加入对 CHX 诱导的细胞毒性有保护作用（P<0.05）。相反，BSO 的加入增强了 CHX 诱导的细胞毒性（P<0.05）。
所测试的 CHX 浓度抑制 U2OS 细胞的生长、增殖和胶原合成。CHX 具有显著的根尖周毒性潜力。GSH 耗竭可能是 CHX 细胞毒性的机制之一。
