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Magnolol inhibits growth of gallbladder cancer cells through the p53 pathway.

Li M, Zhang F, Wang X, Wu X, Zhang B, Zhang N, Wu W, Wang Z, Weng H, Liu S, Gao G, Mu J, Shu Y, Bao R, Cao Y, Lu J, Gu J, Zhu J, Liu Y - Cancer Sci. (2015)

Bottom Line: Magnolol, the major active compound found in Magnolia officinalis has a wide range of clinical applications due to its anti-inflammation and anti-oxidation effects.The results indicated that magnolol could significantly inhibit the growth of GBC cell lines in a dose- and time-dependent manner.In conclusion, our study is the first to report that magnolol has an inhibitory effect on the growth of GBC cells and that this compound may have potential as a novel therapeutic agent for the treatment of GBC.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong, University School of Medicine, Shanghai, China.

No MeSH data available.


Related in: MedlinePlus

Magnolol induces apoptosis in gallbladder cancer (GBC) cells. (a–c) GBC-SD and SGC-996 cells were analyzed by flow cytometry with annexin V–FITC/propidium iodide (PI) staining after magnolol treatment. Annexin V versus PI plots from the gated cells show the populations corresponding to viable (annexin V−/PI−), necrotic (annexin V−/PI+), early apoptotic (annexin V+/PI−), and late apoptotic (annexin V+/PI+) cells. The data are presented as the mean ± SD of three independent experiments. (d) Changes in nuclear morphology during apoptosis were observed by Hoechst 33342 staining and visualized by fluorescence microscopy. *P < 0.05, **P < 0.01 versus control.
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fig02: Magnolol induces apoptosis in gallbladder cancer (GBC) cells. (a–c) GBC-SD and SGC-996 cells were analyzed by flow cytometry with annexin V–FITC/propidium iodide (PI) staining after magnolol treatment. Annexin V versus PI plots from the gated cells show the populations corresponding to viable (annexin V−/PI−), necrotic (annexin V−/PI+), early apoptotic (annexin V+/PI−), and late apoptotic (annexin V+/PI+) cells. The data are presented as the mean ± SD of three independent experiments. (d) Changes in nuclear morphology during apoptosis were observed by Hoechst 33342 staining and visualized by fluorescence microscopy. *P < 0.05, **P < 0.01 versus control.

Mentions: Apoptotic cells with nuclear condensation and fragmentation can be visualized using Hoechst 33258 and DAPI staining. To determine the effects of magnolol treatment on GBC cell apoptosis, Hoechst 33258 staining and flow cytometric analysis were carried out. After GBC cells were exposed to four concentrations of magnolol (0, 10, 20, and 30 μmol/L) for 48 h, the apoptosis index of GBC cells in magnolol-treated groups was markedly higher than in the control group) (Fig.2a–c; *P < 0.05, **P < 0.01, ***P < 0.001). Moreover, GBC cell apoptosis was confirmed using Hoechst 33258 staining, which revealed increased cell membrane permeability and nuclear condensation (Fig.2d). In addition, a decline in the ΔΨm is a characteristic of apoptosis. In this study, the ΔΨm in magnolol-treated GBC cells was examined using rhodamine 123, which can be used to estimate membrane integrity and membrane potential changes. A dose-dependent dissipation of potential was observed in the mitochondrial membranes of GBC cells after 48 h of incubation with magnolol (Fig.3a–c). In addition, magnolol treatment resulted in a time-dependent increase in Bax/Bcl-2 levels, as well as the caspase-9-dependent activation of caspase-3 and of a cleaved form of poly(ADP-ribose) polymerase (Fig.3d). These results indicate that magnolol-induced GBC cell apoptosis occurs through the mitochondria caspase-dependent pathway.


Magnolol inhibits growth of gallbladder cancer cells through the p53 pathway.

Li M, Zhang F, Wang X, Wu X, Zhang B, Zhang N, Wu W, Wang Z, Weng H, Liu S, Gao G, Mu J, Shu Y, Bao R, Cao Y, Lu J, Gu J, Zhu J, Liu Y - Cancer Sci. (2015)

Magnolol induces apoptosis in gallbladder cancer (GBC) cells. (a–c) GBC-SD and SGC-996 cells were analyzed by flow cytometry with annexin V–FITC/propidium iodide (PI) staining after magnolol treatment. Annexin V versus PI plots from the gated cells show the populations corresponding to viable (annexin V−/PI−), necrotic (annexin V−/PI+), early apoptotic (annexin V+/PI−), and late apoptotic (annexin V+/PI+) cells. The data are presented as the mean ± SD of three independent experiments. (d) Changes in nuclear morphology during apoptosis were observed by Hoechst 33342 staining and visualized by fluorescence microscopy. *P < 0.05, **P < 0.01 versus control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4638010&req=5

fig02: Magnolol induces apoptosis in gallbladder cancer (GBC) cells. (a–c) GBC-SD and SGC-996 cells were analyzed by flow cytometry with annexin V–FITC/propidium iodide (PI) staining after magnolol treatment. Annexin V versus PI plots from the gated cells show the populations corresponding to viable (annexin V−/PI−), necrotic (annexin V−/PI+), early apoptotic (annexin V+/PI−), and late apoptotic (annexin V+/PI+) cells. The data are presented as the mean ± SD of three independent experiments. (d) Changes in nuclear morphology during apoptosis were observed by Hoechst 33342 staining and visualized by fluorescence microscopy. *P < 0.05, **P < 0.01 versus control.
Mentions: Apoptotic cells with nuclear condensation and fragmentation can be visualized using Hoechst 33258 and DAPI staining. To determine the effects of magnolol treatment on GBC cell apoptosis, Hoechst 33258 staining and flow cytometric analysis were carried out. After GBC cells were exposed to four concentrations of magnolol (0, 10, 20, and 30 μmol/L) for 48 h, the apoptosis index of GBC cells in magnolol-treated groups was markedly higher than in the control group) (Fig.2a–c; *P < 0.05, **P < 0.01, ***P < 0.001). Moreover, GBC cell apoptosis was confirmed using Hoechst 33258 staining, which revealed increased cell membrane permeability and nuclear condensation (Fig.2d). In addition, a decline in the ΔΨm is a characteristic of apoptosis. In this study, the ΔΨm in magnolol-treated GBC cells was examined using rhodamine 123, which can be used to estimate membrane integrity and membrane potential changes. A dose-dependent dissipation of potential was observed in the mitochondrial membranes of GBC cells after 48 h of incubation with magnolol (Fig.3a–c). In addition, magnolol treatment resulted in a time-dependent increase in Bax/Bcl-2 levels, as well as the caspase-9-dependent activation of caspase-3 and of a cleaved form of poly(ADP-ribose) polymerase (Fig.3d). These results indicate that magnolol-induced GBC cell apoptosis occurs through the mitochondria caspase-dependent pathway.

Bottom Line: Magnolol, the major active compound found in Magnolia officinalis has a wide range of clinical applications due to its anti-inflammation and anti-oxidation effects.The results indicated that magnolol could significantly inhibit the growth of GBC cell lines in a dose- and time-dependent manner.In conclusion, our study is the first to report that magnolol has an inhibitory effect on the growth of GBC cells and that this compound may have potential as a novel therapeutic agent for the treatment of GBC.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong, University School of Medicine, Shanghai, China.

No MeSH data available.


Related in: MedlinePlus