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Tubeimoside-1 induces glioma apoptosis through regulation of Bax/Bcl-2 and the ROS/Cytochrome C/Caspase-3 pathway.

Jia G, Wang Q, Wang R, Deng D, Xue L, Shao N, Zhang Y, Xia X, Zhi F, Yang Y - Onco Targets Ther (2015)

Bottom Line: Tubeimoside-1 (TBMS1) is a natural compound isolated from tubeimoside, which has been widely used as a traditional Chinese herbal medicine.Western blotting showed that TBMS1 induced apoptosis by increasing the expression of Bax and downregulating the level of Bcl-2.Furthermore, we found that TBMS1 induced apoptosis by increasing the concentration of reactive oxygen species through the release of Cytochrome C and activation of Caspase-3.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.

ABSTRACT

Background: Tubeimoside-1 (TBMS1) is a natural compound isolated from tubeimoside, which has been widely used as a traditional Chinese herbal medicine. The purpose of the present study is to investigate the anti-tumor effect and the underling mechanism of TBMS1 on glioma cancer cells.

Methods: The MTT assay was performed to evaluate the effect of TBMS1 on glioma cell proliferation. The fluorescent microscopy and flow cytometry analysis were performed to evaluate the effect of TBMS1 on glioma cell apoptosis. The Western blot analysis was used to evaluate the protein change.

Results: TBMS1 inhibited glioma cancer cell proliferation in a dose- and time-dependent manner. Fluorescent microscopy and flow cytometry analysis demonstrated that TBMS1 induced glioma cell apoptosis in a concentration-dependent manner. Western blotting showed that TBMS1 induced apoptosis by increasing the expression of Bax and downregulating the level of Bcl-2. Furthermore, we found that TBMS1 induced apoptosis by increasing the concentration of reactive oxygen species through the release of Cytochrome C and activation of Caspase-3.

Conclusion: These findings indicate that TBMS1 may be developed as a possible therapeutic agent for the management of glioma.

No MeSH data available.


Related in: MedlinePlus

Effects of TBMS1 on Cytochrome C release and Caspase-3 activation.Notes: The level of Cytochrome C and Caspase-3 expression was evaluated using Western blot analysis. β-actin was used as an internal reference. The quantitative level is shown in histograms and the mean value for the control was set at one. *P<0.05, **P<0.01, ***P<0.001 vs the control group.Abbreviations: TBMS1, Tubeimoside-1; vs, versus.
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f4-ott-8-303: Effects of TBMS1 on Cytochrome C release and Caspase-3 activation.Notes: The level of Cytochrome C and Caspase-3 expression was evaluated using Western blot analysis. β-actin was used as an internal reference. The quantitative level is shown in histograms and the mean value for the control was set at one. *P<0.05, **P<0.01, ***P<0.001 vs the control group.Abbreviations: TBMS1, Tubeimoside-1; vs, versus.

Mentions: We extracted total protein from cancer cells incubated with 15, 20, and 25 μg/mL TBMS1 for 24 hours and analyzed the release of intracellular Cytochrome C and activation of Caspase-3 by Western blotting. As shown in Figure 4, compared with the control group, there was an obvious release of intracellular Cytochrome C and activation of Caspase-3 in the TBMS1 treated groups with a trend of TBMS1 concentration dependence. The result was similar in U87 cells after TBMS1 treatment, as shown in Figure S3.


Tubeimoside-1 induces glioma apoptosis through regulation of Bax/Bcl-2 and the ROS/Cytochrome C/Caspase-3 pathway.

Jia G, Wang Q, Wang R, Deng D, Xue L, Shao N, Zhang Y, Xia X, Zhi F, Yang Y - Onco Targets Ther (2015)

Effects of TBMS1 on Cytochrome C release and Caspase-3 activation.Notes: The level of Cytochrome C and Caspase-3 expression was evaluated using Western blot analysis. β-actin was used as an internal reference. The quantitative level is shown in histograms and the mean value for the control was set at one. *P<0.05, **P<0.01, ***P<0.001 vs the control group.Abbreviations: TBMS1, Tubeimoside-1; vs, versus.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4321652&req=5

f4-ott-8-303: Effects of TBMS1 on Cytochrome C release and Caspase-3 activation.Notes: The level of Cytochrome C and Caspase-3 expression was evaluated using Western blot analysis. β-actin was used as an internal reference. The quantitative level is shown in histograms and the mean value for the control was set at one. *P<0.05, **P<0.01, ***P<0.001 vs the control group.Abbreviations: TBMS1, Tubeimoside-1; vs, versus.
Mentions: We extracted total protein from cancer cells incubated with 15, 20, and 25 μg/mL TBMS1 for 24 hours and analyzed the release of intracellular Cytochrome C and activation of Caspase-3 by Western blotting. As shown in Figure 4, compared with the control group, there was an obvious release of intracellular Cytochrome C and activation of Caspase-3 in the TBMS1 treated groups with a trend of TBMS1 concentration dependence. The result was similar in U87 cells after TBMS1 treatment, as shown in Figure S3.

Bottom Line: Tubeimoside-1 (TBMS1) is a natural compound isolated from tubeimoside, which has been widely used as a traditional Chinese herbal medicine.Western blotting showed that TBMS1 induced apoptosis by increasing the expression of Bax and downregulating the level of Bcl-2.Furthermore, we found that TBMS1 induced apoptosis by increasing the concentration of reactive oxygen species through the release of Cytochrome C and activation of Caspase-3.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.

ABSTRACT

Background: Tubeimoside-1 (TBMS1) is a natural compound isolated from tubeimoside, which has been widely used as a traditional Chinese herbal medicine. The purpose of the present study is to investigate the anti-tumor effect and the underling mechanism of TBMS1 on glioma cancer cells.

Methods: The MTT assay was performed to evaluate the effect of TBMS1 on glioma cell proliferation. The fluorescent microscopy and flow cytometry analysis were performed to evaluate the effect of TBMS1 on glioma cell apoptosis. The Western blot analysis was used to evaluate the protein change.

Results: TBMS1 inhibited glioma cancer cell proliferation in a dose- and time-dependent manner. Fluorescent microscopy and flow cytometry analysis demonstrated that TBMS1 induced glioma cell apoptosis in a concentration-dependent manner. Western blotting showed that TBMS1 induced apoptosis by increasing the expression of Bax and downregulating the level of Bcl-2. Furthermore, we found that TBMS1 induced apoptosis by increasing the concentration of reactive oxygen species through the release of Cytochrome C and activation of Caspase-3.

Conclusion: These findings indicate that TBMS1 may be developed as a possible therapeutic agent for the management of glioma.

No MeSH data available.


Related in: MedlinePlus