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Effectiveness of Panax ginseng on Acute Myocardial Ischemia Reperfusion Injury Was Abolished by Flutamide via Endogenous Testosterone-Mediated Akt Pathway.

Pei L, Shaozhen H, Gengting D, Tingbo C, Liang L, Hua Z - Evid Based Complement Alternat Med (2013)

Bottom Line: RSE (80 mg/kg) significantly inhibited myocardial infarction and CK and LDH activities, while coadministration of flutamide abolished this effect of RSE.Western blot analysis showed that RSE significantly reversed the decreases of expression and activation of PI3K, Akt, and eNOS evoked by ischemia, whereas flutamide attenuated the effects of these protective mechanisms induced by RSE.Our results for the first time indicate that blocking androgen receptor abolishes the ability of Panax ginseng to protect the heart from myocardial I/R injury.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory for Quality Research of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, China.

ABSTRACT
Mechanisms for Panax ginseng's cardioprotective effect against ischemia reperfusion injury involve the estrogen-mediated pathway, but little is known about the role of androgen. A standardized Panax ginseng extract (RSE) was orally given with or without flutamide in a left anterior descending coronary artery ligation rat model. Infarct size, CK and LDH activities were measured. Time-related changes of NO, PI3K/Akt/eNOS signaling, and testosterone concentration were also investigated. RSE (80 mg/kg) significantly inhibited myocardial infarction and CK and LDH activities, while coadministration of flutamide abolished this effect of RSE. NO was increased by RSE and reached a peak after 15 min of ischemia; however, flutamide cotreatment suppressed this elevation. Western blot analysis showed that RSE significantly reversed the decreases of expression and activation of PI3K, Akt, and eNOS evoked by ischemia, whereas flutamide attenuated the effects of these protective mechanisms induced by RSE. RSE completely reversed the dropping of endogenous testosterone level induced by I/R injury. Flutamide plus RSE treatment not only abolished RSE's effect but also produced a dramatic change on endogenous testosterone level after pretreatment and ischemia. Our results for the first time indicate that blocking androgen receptor abolishes the ability of Panax ginseng to protect the heart from myocardial I/R injury.

No MeSH data available.


Related in: MedlinePlus

Effects of RSE and flutamide on time course changes of serum testosterone concentration. Data are shown as mean ± S.E.M, n = 3~5/group at each time point. #P < 0.05, ##P < 0.01, RSE + Flu group compared with Sham group at the corresponding time point; **P < 0.01 IRI group compared with Sham group at the corresponding time point.
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fig7: Effects of RSE and flutamide on time course changes of serum testosterone concentration. Data are shown as mean ± S.E.M, n = 3~5/group at each time point. #P < 0.05, ##P < 0.01, RSE + Flu group compared with Sham group at the corresponding time point; **P < 0.01 IRI group compared with Sham group at the corresponding time point.

Mentions: As shown in Figure 7, the level of testosterone was stable in the sham group during the whole pretreatment and I/R periods. Although 30 min ischemia did not cause a significant decrease in serum testosterone, additional 90 min reperfusion resulted in a significant decrease (23.5% drop compared with the sham group, P < 0.01). Pretreatment with RSE completely suppressed the effect of I/R on serum testosterone levels. Interestingly, after 60 minutes pretreatment, the RSE + Flutamide group showed a significant increase (P < 0.05) in serum testosterone, but this effect was dramatically reversed after 30 minutes of ischemia (P < 0.05) and this reversion remained to the end of 90 min reperfusion.


Effectiveness of Panax ginseng on Acute Myocardial Ischemia Reperfusion Injury Was Abolished by Flutamide via Endogenous Testosterone-Mediated Akt Pathway.

Pei L, Shaozhen H, Gengting D, Tingbo C, Liang L, Hua Z - Evid Based Complement Alternat Med (2013)

Effects of RSE and flutamide on time course changes of serum testosterone concentration. Data are shown as mean ± S.E.M, n = 3~5/group at each time point. #P < 0.05, ##P < 0.01, RSE + Flu group compared with Sham group at the corresponding time point; **P < 0.01 IRI group compared with Sham group at the corresponding time point.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3824556&req=5

fig7: Effects of RSE and flutamide on time course changes of serum testosterone concentration. Data are shown as mean ± S.E.M, n = 3~5/group at each time point. #P < 0.05, ##P < 0.01, RSE + Flu group compared with Sham group at the corresponding time point; **P < 0.01 IRI group compared with Sham group at the corresponding time point.
Mentions: As shown in Figure 7, the level of testosterone was stable in the sham group during the whole pretreatment and I/R periods. Although 30 min ischemia did not cause a significant decrease in serum testosterone, additional 90 min reperfusion resulted in a significant decrease (23.5% drop compared with the sham group, P < 0.01). Pretreatment with RSE completely suppressed the effect of I/R on serum testosterone levels. Interestingly, after 60 minutes pretreatment, the RSE + Flutamide group showed a significant increase (P < 0.05) in serum testosterone, but this effect was dramatically reversed after 30 minutes of ischemia (P < 0.05) and this reversion remained to the end of 90 min reperfusion.

Bottom Line: RSE (80 mg/kg) significantly inhibited myocardial infarction and CK and LDH activities, while coadministration of flutamide abolished this effect of RSE.Western blot analysis showed that RSE significantly reversed the decreases of expression and activation of PI3K, Akt, and eNOS evoked by ischemia, whereas flutamide attenuated the effects of these protective mechanisms induced by RSE.Our results for the first time indicate that blocking androgen receptor abolishes the ability of Panax ginseng to protect the heart from myocardial I/R injury.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory for Quality Research of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, China.

ABSTRACT
Mechanisms for Panax ginseng's cardioprotective effect against ischemia reperfusion injury involve the estrogen-mediated pathway, but little is known about the role of androgen. A standardized Panax ginseng extract (RSE) was orally given with or without flutamide in a left anterior descending coronary artery ligation rat model. Infarct size, CK and LDH activities were measured. Time-related changes of NO, PI3K/Akt/eNOS signaling, and testosterone concentration were also investigated. RSE (80 mg/kg) significantly inhibited myocardial infarction and CK and LDH activities, while coadministration of flutamide abolished this effect of RSE. NO was increased by RSE and reached a peak after 15 min of ischemia; however, flutamide cotreatment suppressed this elevation. Western blot analysis showed that RSE significantly reversed the decreases of expression and activation of PI3K, Akt, and eNOS evoked by ischemia, whereas flutamide attenuated the effects of these protective mechanisms induced by RSE. RSE completely reversed the dropping of endogenous testosterone level induced by I/R injury. Flutamide plus RSE treatment not only abolished RSE's effect but also produced a dramatic change on endogenous testosterone level after pretreatment and ischemia. Our results for the first time indicate that blocking androgen receptor abolishes the ability of Panax ginseng to protect the heart from myocardial I/R injury.

No MeSH data available.


Related in: MedlinePlus