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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 CK and LDH activities in serum after myocardial I/R. The unit of enzymes was expressed as U/L. Data are shown as mean ± S.E.M, n = 5/group. ##P < 0.01, versus Sham group; **P < 0.01 versus IRI group; ∧P < 0.05 versus RSE group.
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fig4: Effects of RSE and flutamide on CK and LDH activities in serum after myocardial I/R. The unit of enzymes was expressed as U/L. Data are shown as mean ± S.E.M, n = 5/group. ##P < 0.01, versus Sham group; **P < 0.01 versus IRI group; ∧P < 0.05 versus RSE group.

Mentions: Besides the evaluation of infarct size induced by I/R, we also measured myocardial enzymes in serum in order to further elucidate the effect of RSE with or without flutamide in rat open chest model. As shown in Figure 4, the activities of CK-MB and LDH in the serum of rats that underwent myocardial I/R (IRI group) were both significantly increased when compared with the sham group without I/R (CK-MB activity: 1476 ± 137 U/L versus 522 ± 214 U/L, P < 0.01; LDH activity: 435 ± 85 U/L versus 67 ± 16 U/L, P < 0.01). Compared with the IRI group, 80 mg/kg RSE treatment significantly inhibited the elevation of CK-MB (894 ± 134 U/L, P < 0.01) or LDH (178 ± 69 U/L, P < 0.01) activities induced by acute I/R injury. The joint use of RSE at 80 mg/kg and flutamide at 10 mg/kg did not significantly suppress the increase of serum CK-MB or LDH activity (1363 ± 199 U/L, 378 ± 45 U/L, compared with IRI group P > 0.05, P > 0.05, resp.). These results also revealed that flutamide significantly abolished the beneficial effect of RSE on the myocardial enzymes (compared with RSE group, CK-MB, P < 0.05 and LDH, P < 0.05) in 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)

Effects of RSE and flutamide on CK and LDH activities in serum after myocardial I/R. The unit of enzymes was expressed as U/L. Data are shown as mean ± S.E.M, n = 5/group. ##P < 0.01, versus Sham group; **P < 0.01 versus IRI group; ∧P < 0.05 versus RSE group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: Effects of RSE and flutamide on CK and LDH activities in serum after myocardial I/R. The unit of enzymes was expressed as U/L. Data are shown as mean ± S.E.M, n = 5/group. ##P < 0.01, versus Sham group; **P < 0.01 versus IRI group; ∧P < 0.05 versus RSE group.
Mentions: Besides the evaluation of infarct size induced by I/R, we also measured myocardial enzymes in serum in order to further elucidate the effect of RSE with or without flutamide in rat open chest model. As shown in Figure 4, the activities of CK-MB and LDH in the serum of rats that underwent myocardial I/R (IRI group) were both significantly increased when compared with the sham group without I/R (CK-MB activity: 1476 ± 137 U/L versus 522 ± 214 U/L, P < 0.01; LDH activity: 435 ± 85 U/L versus 67 ± 16 U/L, P < 0.01). Compared with the IRI group, 80 mg/kg RSE treatment significantly inhibited the elevation of CK-MB (894 ± 134 U/L, P < 0.01) or LDH (178 ± 69 U/L, P < 0.01) activities induced by acute I/R injury. The joint use of RSE at 80 mg/kg and flutamide at 10 mg/kg did not significantly suppress the increase of serum CK-MB or LDH activity (1363 ± 199 U/L, 378 ± 45 U/L, compared with IRI group P > 0.05, P > 0.05, resp.). These results also revealed that flutamide significantly abolished the beneficial effect of RSE on the myocardial enzymes (compared with RSE group, CK-MB, P < 0.05 and LDH, P < 0.05) in 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