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Mitochondria was Involved in Mediating MOPDO-induced Proliferation Inhibition and Apoptosis in HepG2 Cells
Xiao-Wen Gao, Hai-Liang Liu1, Yan-jun Deng2, Si-Yuan Huang, Li-Zhi Xu, Xiao-Ning Zhao, Jing-Gao1*, Qi-Zheng Yao2
School of Life Science, Nanjing University, Nanjing 210093, China; 1School of Pharmacy, Jiangsu University, Zhenjiang 212013, China;2School of Pharmacy, China Pharmaceutical University, Nanjing 210009, China
Abstract: To investigate the anticancer effect of a newly synthesized 6-Methyl-4-(2-fluoro-3，5-di-O-benzoyl-1-β-D-ribofuranosyl)-[1，2，5]-oxadiazolo[3，4-d]pyrimidine-5(4H)，7(6H)-dione 1-oxide (MOPDO)， a nitric oxide donating-compound derivated from nucleotide analogue， in human hepatoma cell line HepG2. Cell proliferation was assessed by MTT assay and morphological observation. Cell apoptotic rate was detected by flow cytometry (FCM) following annexin-V/PI staining. Mitochondrial membrane potential was observed by fluorescence microscopy with JC-1 loading. NO levels were measured by quantifying the content of nitrite and nitrate in the cell culture medium. The results showed that MOPDO inhibited the HepG2 cell viability significantly in a both concentration- and time-dependent manner. Apoptosis properties were observed， as characterized by annexin-V/PI double staining， showing that apoptotic rate increased in a concentration- and time-dependent manner. Moreover， MOPDO caused a loss of mitochondrial membrane potential in a dose-dependent manner. In addition， NO assay indicated that MOPDO elevated NO level in a concentration-dependent manner. The above data indicated that mitochondria might be involved in mediating the MOPDO-induced proliferation inhibition and apoptosis in HepG2 cells.
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