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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

Infarct size after myocardial I/R injury. (a) Representative photos of TTC stained left ventricle slices. Deep red-staining areas indicate normal tissue, and unstained pale areas indicate infarct tissue. (b) Bar chart of myocardial infarct size determined by TTC staining. Data are shown as mean ± S.E.M, n = 6~7/group. ##P < 0.01 versus Sham group, **P < 0.01 versus IRI group, ∧∧P < 0.01 versus RSE group.
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fig3: Infarct size after myocardial I/R injury. (a) Representative photos of TTC stained left ventricle slices. Deep red-staining areas indicate normal tissue, and unstained pale areas indicate infarct tissue. (b) Bar chart of myocardial infarct size determined by TTC staining. Data are shown as mean ± S.E.M, n = 6~7/group. ##P < 0.01 versus Sham group, **P < 0.01 versus IRI group, ∧∧P < 0.01 versus RSE group.

Mentions: Occluding and releasing the LAD coronary artery of SD rats is a widely used model for antimyocardial I/R injury research. The severity of I/R injury can be assessed by measuring the size of infarct area (myocardial infarct size). As shown in Figure 3, the myocardial infarct size produced by 30 min ischemia and 90 min reperfusion in IRI group was 10.5 ± 2.20%. Orally given 60 min before the acute ischemia, RSE at 80 mg/kg exhibited significant protection to rat hearts against I/R injury with an infarct size of 0.3 ± 0.32% (compared with IRI group, P < 0.01). Combined administration of RSE and flutamide (at 80 mg/kg and 10 mg/kg, resp.) did not induce any significant reduction in myocardial infarct size (10.7 ± 3.56%, P < 0.05 and P < 0.01, compared with IRI or RSE group, resp.). This clearly indicates that flutamide abolished the protective effect of RSE against I/R injury.


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)

Infarct size after myocardial I/R injury. (a) Representative photos of TTC stained left ventricle slices. Deep red-staining areas indicate normal tissue, and unstained pale areas indicate infarct tissue. (b) Bar chart of myocardial infarct size determined by TTC staining. Data are shown as mean ± S.E.M, n = 6~7/group. ##P < 0.01 versus Sham group, **P < 0.01 versus IRI group, ∧∧P < 0.01 versus RSE group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Infarct size after myocardial I/R injury. (a) Representative photos of TTC stained left ventricle slices. Deep red-staining areas indicate normal tissue, and unstained pale areas indicate infarct tissue. (b) Bar chart of myocardial infarct size determined by TTC staining. Data are shown as mean ± S.E.M, n = 6~7/group. ##P < 0.01 versus Sham group, **P < 0.01 versus IRI group, ∧∧P < 0.01 versus RSE group.
Mentions: Occluding and releasing the LAD coronary artery of SD rats is a widely used model for antimyocardial I/R injury research. The severity of I/R injury can be assessed by measuring the size of infarct area (myocardial infarct size). As shown in Figure 3, the myocardial infarct size produced by 30 min ischemia and 90 min reperfusion in IRI group was 10.5 ± 2.20%. Orally given 60 min before the acute ischemia, RSE at 80 mg/kg exhibited significant protection to rat hearts against I/R injury with an infarct size of 0.3 ± 0.32% (compared with IRI group, P < 0.01). Combined administration of RSE and flutamide (at 80 mg/kg and 10 mg/kg, resp.) did not induce any significant reduction in myocardial infarct size (10.7 ± 3.56%, P < 0.05 and P < 0.01, compared with IRI or RSE group, resp.). This clearly indicates that flutamide abolished the protective effect of RSE against I/R injury.

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