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Objective: 5 - allyl-7 - difluoromethylene chrysin (5-allyl-7-gen-difluoromethylene chrysin ADFMChR) inhibit the in vitro culture of human ovarian cancer cell lines CoC1 cell growth and induction of apoptosis; explore its mechanism of action is involved PPARγ activating. Method: in vitro culture of human ovarian cancer CoC1 cells, MTT colorimetric determination of cell proliferation activity; cell counting method to detect cell survival, cell growth curve; soft agar colony formation assay cell anchorage-independent growth; PI staining streaming is cytometry (FCM) quantitative analysis of the degree of apoptosis; DNA gel electrophoresis confirmatory induced apoptosis; Western blot to detect cell of PPARγ, NF-κB, Bcl-2, Bax protein expression. Results: MTT method results show: the concentration 1.0,3.0,10.0,30.0,100.0 μmol / L of ADFMChR 100.0μmol / L ChR processing human ovarian cancer CoC1 cells 48 hours, the cell inhibition rate were 26.4 %, 40.6%, 51.3%, 68.4%, 75.8% and 57.5%, the IC50 value 7.26μmol / L, and ADFMChR (100.0μmol / L) inhibition rate (75.8%) was higher than ChR (57.5%) (P lt ; 0.01). Cell count results show: 1.0,3.0,10.0,30.0,100.0 μmol / L ADFMChR inhibit CoC1 cell growth in a concentration-dependent manner, 30μmol / L ADFMChR Coc1 cell population doubling time can be extended from 28.5h to 39.6h. Soft agar colony forming assay results the ADFMChR1.0 3.0,10.0,30.0,100.0 μmol / L ChR100.0μmol / L respectively, deal with a set of eight days human ovarian cancer COC1 cells fall inhibition rates were 12.6%, 32.4%, 56.6%, 83.5%, 90.1% and 75.3%, ADFMChR (100.0 μmol / L) the set drop than ChR inhibition rate (90.1%) (75.3%) (P lt; 0.01). ADFMChR (30.0μmol / L) to handle CoC1 cells 48h, agarose gel electrophoresis showed typical \The PI staining FCM the analysis found ADFMChR dose-dependent induced CoC1 cell apoptosis, ADFMChR (10.0,30.0 μmol / L) treatment CoC1 cells 48h, the apoptosis rate of 33.1% and 73.7%, respectively, were higher than the corresponding concentrations chrysin induced withered death rate (21.7%, 40.0%) (P lt; 0.01). Western blot analysis shows: The 0.3,3.0,30.0 μmol / L ADFMChR CoC1 cells for 24 h, compared with the blank control group: of PPARγ expression were increased by 10.9%, 31.5%, 48.5%; expression of NF-κB were down 5.0%, 29.1%, 43.5%; Bcl-2 expression were reduced by 10.5%, 31.1%, 56.5%; Bax Expressions were raised by 4.8%, 34.5% and 65.1%, respectively. ADFMChR (30.0μmol / L), respectively handle CoC1 cells 6,12,24 h, compared with the blank control group: PPARγ expression were increased by 23.1%, 54.0%, 65.0%; Bax Expressions were raised by 8.6%, 27.9%, 60.1%; NF-κB expression were down 11.5%, 29.0%, 54.8%; Bcl-2 expression were down 26.9%, 49.4% and 61.7%, respectively. Conclusions: 1) ADFMChR inhibition of in vitro cultured human the ovarian cancer CoC1 cell growth, and a dose-dependent manner. 2) ADFMChR has induced human of ovarian cancer CoC1 cells apoptosis. 3) ADFMChR induced the ovarian cancer CoC1 cell apoptosis associated with activation of PPARγ, inhibition of NF-κB and Bcl-2 expression of Bax protein expression.
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