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Ginsenoside rb1 protects neonatal rat cardiomyocytes from hypoxia/ischemia induced apoptosis and inhibits activation of the mitochondrial apoptotic pathway.

Yan X, Tian J, Wu H, Liu Y, Ren J, Zheng S, Zhang C, Yang C, Li Y, Wang S - Evid Based Complement Alternat Med (2014)

Bottom Line: GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I.It also reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Beijing Haidian Hospital (Haidian Section of Peking University Third Hospital), 29 Zhongguancun Dajie, Haidian District, Beijing 100080, China ; Postdoctoral Workstation of the Zhongguancun Haidian Science Park, NO. 6, Sijiqing Road, Haidian District, Beijing 100195, China.

ABSTRACT
Aim. To investigate the effect of Ginsenoside Rb1 (GS-Rb1) on hypoxia/ischemia (H/I) injury in cardiomyocytes in vitro and the mitochondrial apoptotic pathway mediated mechanism. Methods. Neonatal rat cardiomyocytes (NRCMs) for the H/I groups were kept in DMEM without glucose and serum, and were placed into a hypoxic jar for 24 h. GS-Rb1 at concentrations from 2.5 to 40 µM was given during hypoxic period for 24 h. NRCMs injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. Cell apoptosis, ROS accumulation, and mitochondrial membrane potential (MMP) were assessed by flow cytometry. Cytosolic translocation of mitochondrial cytochrome c and Bcl-2 family proteins were determined by Western blot. Caspase-3 and caspase-9 activities were determined by the assay kit. Results. GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I. It also reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst. Moreover, GS-Rb1 markedly decreased the translocation of cytochrome c from the mitochondria to the cytosol, increased the Bcl-2/ Bax ratio, and preserved mitochondrial transmembrane potential (ΔΨm). Its administration also inhibited activities of caspase-9 and caspase-3. Conclusion. Administration of GS-Rb1 during H/I in vitro is involved in cardioprotection by inhibiting apoptosis, which may be due to inhibition of the mitochondrial apoptotic pathway.

No MeSH data available.


Related in: MedlinePlus

Effect of GS-Rb1 on Bcl-2 and Bax changes induced by H/I. NRCMs were cotreated with or without GS-Rb1 (5, 10, 20, and 40 μM) during H/I for 24 h. (a) The protein levels of Bcl-2 and Bax were quantified by Western blot. (b) Quantitative data analysis for each group. (c) Bcl-2/Bax protein expression ratio in each group. Error bars represent mean ± SD. ∗∗∗P < 0.001 versus Bcl-2 in control group; ##P < 0.01 versus Bax in control group; +P < 0.05, ++P < 0.01, and +++P < 0.001 versus Bcl-2 in H/I group; &P < 0.05 and &&P < 0.01 versus Bax in H/I group.
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fig6: Effect of GS-Rb1 on Bcl-2 and Bax changes induced by H/I. NRCMs were cotreated with or without GS-Rb1 (5, 10, 20, and 40 μM) during H/I for 24 h. (a) The protein levels of Bcl-2 and Bax were quantified by Western blot. (b) Quantitative data analysis for each group. (c) Bcl-2/Bax protein expression ratio in each group. Error bars represent mean ± SD. ∗∗∗P < 0.001 versus Bcl-2 in control group; ##P < 0.01 versus Bax in control group; +P < 0.05, ++P < 0.01, and +++P < 0.001 versus Bcl-2 in H/I group; &P < 0.05 and &&P < 0.01 versus Bax in H/I group.

Mentions: Bcl-2 family proteins have a function in mitochondria mediated apoptosis. Expression of antiapoptotic Bcl-2 and proapoptotic Bax proteins were analyzed by Western blot after H/I and GS-Rb1 treatment. Compared with the control group, H/I significantly increased Bax expression and decreased Bcl-2. The ratio of Bcl-2 to Bax decreased over 10-fold. With GS-Rb1 cotreatment, increased levels of Bcl-2 and a marked reduction in Bax were observed in a dose-dependent manner (Figures 6(a), 6(b), and 6(c)). Thus, GS-Rb1 inhibits apoptosis induced by H/I by upregulating the ratio of Bcl-2 to Bax.


Ginsenoside rb1 protects neonatal rat cardiomyocytes from hypoxia/ischemia induced apoptosis and inhibits activation of the mitochondrial apoptotic pathway.

Yan X, Tian J, Wu H, Liu Y, Ren J, Zheng S, Zhang C, Yang C, Li Y, Wang S - Evid Based Complement Alternat Med (2014)

Effect of GS-Rb1 on Bcl-2 and Bax changes induced by H/I. NRCMs were cotreated with or without GS-Rb1 (5, 10, 20, and 40 μM) during H/I for 24 h. (a) The protein levels of Bcl-2 and Bax were quantified by Western blot. (b) Quantitative data analysis for each group. (c) Bcl-2/Bax protein expression ratio in each group. Error bars represent mean ± SD. ∗∗∗P < 0.001 versus Bcl-2 in control group; ##P < 0.01 versus Bax in control group; +P < 0.05, ++P < 0.01, and +++P < 0.001 versus Bcl-2 in H/I group; &P < 0.05 and &&P < 0.01 versus Bax in H/I group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig6: Effect of GS-Rb1 on Bcl-2 and Bax changes induced by H/I. NRCMs were cotreated with or without GS-Rb1 (5, 10, 20, and 40 μM) during H/I for 24 h. (a) The protein levels of Bcl-2 and Bax were quantified by Western blot. (b) Quantitative data analysis for each group. (c) Bcl-2/Bax protein expression ratio in each group. Error bars represent mean ± SD. ∗∗∗P < 0.001 versus Bcl-2 in control group; ##P < 0.01 versus Bax in control group; +P < 0.05, ++P < 0.01, and +++P < 0.001 versus Bcl-2 in H/I group; &P < 0.05 and &&P < 0.01 versus Bax in H/I group.
Mentions: Bcl-2 family proteins have a function in mitochondria mediated apoptosis. Expression of antiapoptotic Bcl-2 and proapoptotic Bax proteins were analyzed by Western blot after H/I and GS-Rb1 treatment. Compared with the control group, H/I significantly increased Bax expression and decreased Bcl-2. The ratio of Bcl-2 to Bax decreased over 10-fold. With GS-Rb1 cotreatment, increased levels of Bcl-2 and a marked reduction in Bax were observed in a dose-dependent manner (Figures 6(a), 6(b), and 6(c)). Thus, GS-Rb1 inhibits apoptosis induced by H/I by upregulating the ratio of Bcl-2 to Bax.

Bottom Line: GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I.It also reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Beijing Haidian Hospital (Haidian Section of Peking University Third Hospital), 29 Zhongguancun Dajie, Haidian District, Beijing 100080, China ; Postdoctoral Workstation of the Zhongguancun Haidian Science Park, NO. 6, Sijiqing Road, Haidian District, Beijing 100195, China.

ABSTRACT
Aim. To investigate the effect of Ginsenoside Rb1 (GS-Rb1) on hypoxia/ischemia (H/I) injury in cardiomyocytes in vitro and the mitochondrial apoptotic pathway mediated mechanism. Methods. Neonatal rat cardiomyocytes (NRCMs) for the H/I groups were kept in DMEM without glucose and serum, and were placed into a hypoxic jar for 24 h. GS-Rb1 at concentrations from 2.5 to 40 µM was given during hypoxic period for 24 h. NRCMs injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. Cell apoptosis, ROS accumulation, and mitochondrial membrane potential (MMP) were assessed by flow cytometry. Cytosolic translocation of mitochondrial cytochrome c and Bcl-2 family proteins were determined by Western blot. Caspase-3 and caspase-9 activities were determined by the assay kit. Results. GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I. It also reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst. Moreover, GS-Rb1 markedly decreased the translocation of cytochrome c from the mitochondria to the cytosol, increased the Bcl-2/ Bax ratio, and preserved mitochondrial transmembrane potential (ΔΨm). Its administration also inhibited activities of caspase-9 and caspase-3. Conclusion. Administration of GS-Rb1 during H/I in vitro is involved in cardioprotection by inhibiting apoptosis, which may be due to inhibition of the mitochondrial apoptotic pathway.

No MeSH data available.


Related in: MedlinePlus