文献类型：期刊文献

英文题名：In vitro cytotoxicity and induction of apoptosis by silica nanoparticles in human HepG2 hepatoma cells

作者：Lu, Xun;Qian, Jiangchao[2];Zhou, Huanjun;Gan, Qi;Tang, Wei[2];Lu, Jingxiong;Yuan, Yuan[1,2];Liu, Changsheng[1,2]

机构：[1]E China Univ Sci & Technol, Engn Res Ctr Biomed Mat, Minist Educ, Key Lab Ultrafine Mat, Shanghai 200237, Peoples R China;[2]E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China

年份：2011

卷号：6

起止页码：1889

外文期刊名：INTERNATIONAL JOURNAL OF NANOMEDICINE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000294548900001)】；

基金：The authors appreciate the financial support from the National Natural Science Foundation of China, the Shanghai Nanotechnology Special Foundation, the Fundamental Research Funds for the Central Universities and Program for Changjiang Scholars, and the Innovative Research Team in University.

语种：英文

外文关键词：silica nanoparticles; cytotoxicity; apoptosis; HepG2 cells; mitochondrial-dependent pathway; oxidative stress

摘要：Background: Silica nanoparticles have been discovered to exert cytotoxicity and induce apoptosis in normal human cells. However, until now, few studies have investigated the cytotoxicity of silica nanoparticles in tumor cells. Methods: This study investigated the cytotoxicity of 7-50 nm silica nanoparticles in human HepG2 hepatoma cells, using normal human L-02 hepatocytes as a control. Cell nucleus morphology changes, cellular uptake, and expression of procaspase-9, p53, Bcl-2, and Bax, as well as the activity of caspase-3, and intracellular reactive oxygen species and glutathione levels in the silica nanoparticle-treated cells, were analyzed. Results: The antitumor activity of the silica nanoparticles was closely related to particle size, and the antiproliferation activity decreased in the order of 20 nm > 7 nm > 50 nm. The silica nanoparticles were also cytotoxic in a dose- and time-dependent manner. However, the silica nanoparticles showed only slight toxicity in the L-02 control cells, Moreover, in HepG2 cells, oxidative stress and apoptosis were induced after exposure to 7-20 nm silica nanoparticles. Expression of p53 and caspase-3 increased, and expression of Bcl-2 and procaspase-9 decreased in a dose- dependent manner, whereas the expression of Bax was not significantly changed. Conclusion: A mitochondrial-dependent pathway triggered by oxidative stress mediated by reactive oxygen species may be involved in apoptosis induced by silica nanoparticles, and hence cytotoxicity in human HepG2 hepatic cancer cells.