N-4-Hydroxyphengl Retinode enhances the killing effect of cisplatin on ovarian cancer cells

Objective:To study the effect of N-4-Hydroxyphengl Retinode (4-HPR) combined with cisplatin on ovarian cancer cell apoptosis and ATP production.Methods:Ovarian cancer SKOV3 cells were cultured and divided into control group treated by medium not containing serum or drugs, DPP group treated by cispla...

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Veröffentlicht in:海南医科大学学报(英文版) 2016, Vol.22 (18), p.15-18
Hauptverfasser: Guan-Li Xu, Zi-Jun Yan, Bo Yang, Xiu-Zhen Zhu
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Sprache:eng
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Zusammenfassung:Objective:To study the effect of N-4-Hydroxyphengl Retinode (4-HPR) combined with cisplatin on ovarian cancer cell apoptosis and ATP production.Methods:Ovarian cancer SKOV3 cells were cultured and divided into control group treated by medium not containing serum or drugs, DPP group treated by cisplatin with final concentration of 5 μmol/L, and DPP+HPR group treated by cisplatin with final concentration of 5 μmol/L and 5 μmol/L 4-HPR. 12 h and 24 h after treatment, the number of viable apoptotic cells and non-viable apoptotic cells, ATP production as well as the expression levels of apoptotic molecules CytC, Caspase-3, Grp78 and Caspase-12 in the cells were determined.Results: The number of viable apoptotic cells and non-viable apoptotic cells per 100 cells of DPP group and DPP+HPR group were significantly more than those of control group, ATP production per mg total protein were significantly lower than those of control group, and CytC, Caspase-3, Grp78 and Caspase-12 levels per mg total protein were significantly higher than those of control group; the number of viable apoptotic cells and non-viable apoptotic cells per 100 cells of DPP+HPR group were significantly more than those of DPP group, ATP production per mg total protein was significantly lower than that of DPP group, and CytC, Caspase-3, Grp78 and Caspase-12 levels per mg total protein were significantly higher than those of DPP group.Conclusion:4-HPR can enhance the killing effect of cisplatin on ovarian cancer cells through the mitochondrial apoptosis pathway and endoplasmic reticulum apoptosis pathway.
ISSN:1007-1237