OBJECTIVE: To study the effects of ursolic acid (UA), apentacyclic triterpene acid, on MCF-7 cell apoptosis. METHODS: MCF-7 cells were cultured with different concentrations of UA. Viability of UA-induced MCF-7 cells was evaluated by MTT assay. Cell cycle and sub-G1 peak were performed by FCM. Morphologic changes of UA-treated cells were observed by light microscope. Apoptotic cells with condensed or fragmented nuclei were visualized by Ho33258 and PI staining by a fluorescence microscope (EX: U.V., Green light). p 53 protein expression was analyzed by fluorescence immunohistochemical method (SABC-Cy3). RESULT: 24 hours after UA treatment, inhibition of MCF-7 cell proliferation was concentration-dependent. The IC50 value for UA was 22.6 +/- 3.0 micromol/L. Cell cycle analysis by FCM showed that 50 micromol/L of the drug arrested MCF-7 cell cycle at G0-G1 phase. Morphological changes of MCF-7 cells exhibited many of the hallmark features of apoptosis, including condensation of chromatin and DNA fragmentation. UA increased p 53 protein expression. CONCLUSION: The results suggest that UA evokes MCF-7 cell apoptosis is correlation with the up-regulation of p 53. The study indicated that UA might be a potential Chinese medical component for breast neoplasm.
OBJECTIVE: To study the effects of ursolic acid (UA), apentacyclic triterpene acid, on MCF-7 cell apoptosis. METHODS: MCF-7 cells were cultured with different concentrations of UA. Viability of UA-induced MCF-7 cells was evaluated by MTT assay. Cell cycle and sub-G1 peak were performed by FCM. Morphologic changes of UA-treated cells were observed by light microscope. Apoptotic cells with condensed or fragmented nuclei were visualized by Ho33258 and PI staining by a fluorescence microscope (EX: U.V., Green light). p 53 protein expression was analyzed by fluorescence immunohistochemical method (SABC-Cy3). RESULT: 24 hours after UA treatment, inhibition of MCF-7 cell proliferation was concentration-dependent. The IC50 value for UA was 22.6 +/- 3.0 micromol/L. Cell cycle analysis by FCM showed that 50 micromol/L of the drug arrested MCF-7 cell cycle at G0-G1 phase. Morphological changes of MCF-7 cells exhibited many of the hallmark features of apoptosis, including condensation of chromatin and DNA fragmentation. UA increased p 53 protein expression. CONCLUSION: The results suggest that UA evokes MCF-7 cell apoptosis is correlation with the up-regulation of p 53. The study indicated that UA might be a potential Chinese medical component for breast neoplasm.