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Bo Zhao - One of the best experts on this subject based on the ideXlab platform.
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Ginsenoside Rb1 preconditioning enhances enos expression and attenuates myocardial ischemia reperfusion injury in diabetic rats
BioMed Research International, 2011Co-Authors: Bo Zhao, Yang Wu, Li Zhang, Jinjin XuAbstract:Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
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Ginsenoside Rb1 Preconditioning Enhances eNOS Expression and Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats
BioMed Research International, 2011Co-Authors: Bo Zhao, Yang Wu, Li Zhang, Jinjin XuAbstract:Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
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protective effect of Ginsenoside Rb1 against myocardial ischemia reperfusion injury in streptozotocin induced diabetic rats
Molecular Biology Reports, 2011Co-Authors: Yang Wu, Li Zhang, Jinjin Xu, Bo ZhaoAbstract:The objective of the current study is to investigate whether Ginsenoside Rb1, a major pharmacological extract of ginseng that could attenuate myocardial ischemia reperfusion (MI/R) injury in non-diabetic myocardium, can attenuate MI/R injury in diabetes that are more vulnerable to ischemic insult. Rats were divided into seven groups: (i) diabetic sham, (ii) diabetic, (iii) normal, (iv) diabetic + Ginsenoside Rb1, (v) diabetic + wortmannin, (vi) diabetic + wortmannin + Ginsenoside Rb1, (vii) diabetic sham + wortmannin. Ginsenoside Rb1 and/or wortmannin were administered prior to inducing MI/R (30 min of coronary artery occlusion followed by 120 min reperfusion). At the end of the experiment, postischemic myocardial infarct size was significantly higher in the diabetic untreated group as compared to normal (P < 0.05), accompanied with increased myocardial apoptosis, elevated plasma CK-MB and LDH release and reduced blood pressure. Ginsenoside Rb1 reduced infarct size, cardiomyocyte apoptosis and caspase-3 activity compared to the diabetic group. The cardioprotective effects of Ginsenoside Rb1 were cancelled by wortmannin. Ginsenoside Rb1 significantly upregulated phosphorylated Akt expression, which was attenuated by wortmannin. Ginsenoside Rb1 exerts cardioprotective effects against MI/R injury in diabetic rats, which is partly through activation of phosphatidylinositol 3-kinase (PI3 K)/Akt pathway. Thus this study shows a novel pharmacological preconditioning with Ginsenoside Rb1 in the diabetic myocardium.
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Protective effect of Ginsenoside Rb1 against myocardial ischemia/reperfusion injury in streptozotocin-induced diabetic rats
Molecular Biology Reports, 2010Co-Authors: Yang Wu, Li Zhang, Jinjin Xu, Bo ZhaoAbstract:The objective of the current study is to investigate whether Ginsenoside Rb1, a major pharmacological extract of ginseng that could attenuate myocardial ischemia reperfusion (MI/R) injury in non-diabetic myocardium, can attenuate MI/R injury in diabetes that are more vulnerable to ischemic insult. Rats were divided into seven groups: (i) diabetic sham, (ii) diabetic, (iii) normal, (iv) diabetic + Ginsenoside Rb1, (v) diabetic + wortmannin, (vi) diabetic + wortmannin + Ginsenoside Rb1, (vii) diabetic sham + wortmannin. Ginsenoside Rb1 and/or wortmannin were administered prior to inducing MI/R (30 min of coronary artery occlusion followed by 120 min reperfusion). At the end of the experiment, postischemic myocardial infarct size was significantly higher in the diabetic untreated group as compared to normal (P < 0.05), accompanied with increased myocardial apoptosis, elevated plasma CK-MB and LDH release and reduced blood pressure. Ginsenoside Rb1 reduced infarct size, cardiomyocyte apoptosis and caspase-3 activity compared to the diabetic group. The cardioprotective effects of Ginsenoside Rb1 were cancelled by wortmannin. Ginsenoside Rb1 significantly upregulated phosphorylated Akt expression, which was attenuated by wortmannin. Ginsenoside Rb1 exerts cardioprotective effects against MI/R injury in diabetic rats, which is partly through activation of phosphatidylinositol 3-kinase (PI3 K)/Akt pathway. Thus this study shows a novel pharmacological preconditioning with Ginsenoside Rb1 in the diabetic myocardium.
Ying Jiang - One of the best experts on this subject based on the ideXlab platform.
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Ginsenoside Rb1 attenuates intestinal ischemia reperfusion induced renal injury by activating nrf2 are pathway
Molecules, 2012Co-Authors: Qingtao Meng, Ying JiangAbstract:Intestinal ischemia reperfusion (IIR) is a serious clinical condition associated with simultaneous multiple organ dysfunction. The aim of this study was to investigate the effects of Ginsenoside Rb1 on IIR induced renal injury in mice. An intestinal ischemia reperfusion mouse model was established by superior mesenteric artery (SMA) occlusion for 45 min, followed by reperfusion for 2 h. IIR induced renal injury characterized by increase of BUN, Cr and NGAL in serum, MDA levels and decrease of SOD levels in the renal tissues. Ginsenoside Rb1 (30, 60 mg/kg) given intraperitoneally before reperfusion attennuated renal injury, which was associated with decrease of BUN, Cr and NGAL in serum, MDA levels and increase of SOD levels in the renal tissues. Furthermore, the immunohistochemistry and Western blot data showed that Ginsenoside Rb1 dramatically reversed IIR induced renal injury, associated with upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in renal tissues. Our data suggests that Ginsenoside Rb1 attenuates acute renal injury induced by intestinal ischemia reperfusion by activating the Nrf2/ARE pathway.
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Ginsenoside Rb1 Attenuates Intestinal Ischemia Reperfusion Induced Renal Injury by Activating Nrf2/ARE Pathway
Molecules, 2012Co-Authors: Qingtao Meng, Ying JiangAbstract:Intestinal ischemia reperfusion (IIR) is a serious clinical condition associated with simultaneous multiple organ dysfunction. The aim of this study was to investigate the effects of Ginsenoside Rb1 on IIR induced renal injury in mice. An intestinal ischemia reperfusion mouse model was established by superior mesenteric artery (SMA) occlusion for 45 min, followed by reperfusion for 2 h. IIR induced renal injury characterized by increase of BUN, Cr and NGAL in serum, MDA levels and decrease of SOD levels in the renal tissues. Ginsenoside Rb1 (30, 60 mg/kg) given intraperitoneally before reperfusion attennuated renal injury, which was associated with decrease of BUN, Cr and NGAL in serum, MDA levels and increase of SOD levels in the renal tissues. Furthermore, the immunohistochemistry and Western blot data showed that Ginsenoside Rb1 dramatically reversed IIR induced renal injury, associated with upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in renal tissues. Our data suggests that Ginsenoside Rb1 attenuates acute renal injury induced by intestinal ischemia reperfusion by activating the Nrf2/ARE pathway.
Yu Fu - One of the best experts on this subject based on the ideXlab platform.
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biotransformation of Ginsenoside Rb1 to Ginsenoside rg3 by endophytic bacterium burkholderia sp ge 17 7 isolated from panax ginseng
Journal of Applied Microbiology, 2017Co-Authors: Yu FuAbstract:Aims To isolate a novel endophytic bacterium from Panax ginseng that could have excellent properties in converting Ginsenoside Rb1 to Ginsenoside Rg3. Methods and Results Based on a 16S rDNA gene sequence, the strain named GE 17-7 was identified as Burkholderia sp. This strain has shown the highest activity in converting Ginsenoside Rb1 to 20(S)-Ginsenoside Rg3. During the biotransformation of Ginsenoside Rb1, the final metabolite was identified by nuclear magnetic resonance analysis and the transformation pathway of Ginsenoside Rb1 was also identified by thin-layer chromatography and high performance liquid chromatography analysis in this study. Conclusions We have successfully isolated a β-glucosidase-producing endophytic bacterium GE 17-7 from P. ginseng. Ginsenoside Rg3 was produced by strain GE 17-7 from Ginsenoside Rb1 via Ginsenoside Rd. Significance and Impact of the Study This is the first report of the conversion of major Ginsenoside Rb1 into minor Ginsenoside Rg3 by fermentation with Burkholderia sp. endophytic bacteria in P. ginseng. These results suggest a new preparation method for Ginsenoside Rg3 using strain GE 17-7 in the pharmaceutical industry.
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Biotransformation of Ginsenoside Rb1 to Ginsenoside Rg3 by endophytic bacterium Burkholderia sp. GE 17‐7 isolated from Panax ginseng
Journal of Applied Microbiology, 2017Co-Authors: Yu FuAbstract:Aims To isolate a novel endophytic bacterium from Panax ginseng that could have excellent properties in converting Ginsenoside Rb1 to Ginsenoside Rg3. Methods and Results Based on a 16S rDNA gene sequence, the strain named GE 17-7 was identified as Burkholderia sp. This strain has shown the highest activity in converting Ginsenoside Rb1 to 20(S)-Ginsenoside Rg3. During the biotransformation of Ginsenoside Rb1, the final metabolite was identified by nuclear magnetic resonance analysis and the transformation pathway of Ginsenoside Rb1 was also identified by thin-layer chromatography and high performance liquid chromatography analysis in this study. Conclusions We have successfully isolated a β-glucosidase-producing endophytic bacterium GE 17-7 from P. ginseng. Ginsenoside Rg3 was produced by strain GE 17-7 from Ginsenoside Rb1 via Ginsenoside Rd. Significance and Impact of the Study This is the first report of the conversion of major Ginsenoside Rb1 into minor Ginsenoside Rg3 by fermentation with Burkholderia sp. endophytic bacteria in P. ginseng. These results suggest a new preparation method for Ginsenoside Rg3 using strain GE 17-7 in the pharmaceutical industry.
Jinjin Xu - One of the best experts on this subject based on the ideXlab platform.
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Ginsenoside Rb1 preconditioning enhances enos expression and attenuates myocardial ischemia reperfusion injury in diabetic rats
BioMed Research International, 2011Co-Authors: Bo Zhao, Yang Wu, Li Zhang, Jinjin XuAbstract:Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
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Ginsenoside Rb1 Preconditioning Enhances eNOS Expression and Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats
BioMed Research International, 2011Co-Authors: Bo Zhao, Yang Wu, Li Zhang, Jinjin XuAbstract:Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
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protective effect of Ginsenoside Rb1 against myocardial ischemia reperfusion injury in streptozotocin induced diabetic rats
Molecular Biology Reports, 2011Co-Authors: Yang Wu, Li Zhang, Jinjin Xu, Bo ZhaoAbstract:The objective of the current study is to investigate whether Ginsenoside Rb1, a major pharmacological extract of ginseng that could attenuate myocardial ischemia reperfusion (MI/R) injury in non-diabetic myocardium, can attenuate MI/R injury in diabetes that are more vulnerable to ischemic insult. Rats were divided into seven groups: (i) diabetic sham, (ii) diabetic, (iii) normal, (iv) diabetic + Ginsenoside Rb1, (v) diabetic + wortmannin, (vi) diabetic + wortmannin + Ginsenoside Rb1, (vii) diabetic sham + wortmannin. Ginsenoside Rb1 and/or wortmannin were administered prior to inducing MI/R (30 min of coronary artery occlusion followed by 120 min reperfusion). At the end of the experiment, postischemic myocardial infarct size was significantly higher in the diabetic untreated group as compared to normal (P < 0.05), accompanied with increased myocardial apoptosis, elevated plasma CK-MB and LDH release and reduced blood pressure. Ginsenoside Rb1 reduced infarct size, cardiomyocyte apoptosis and caspase-3 activity compared to the diabetic group. The cardioprotective effects of Ginsenoside Rb1 were cancelled by wortmannin. Ginsenoside Rb1 significantly upregulated phosphorylated Akt expression, which was attenuated by wortmannin. Ginsenoside Rb1 exerts cardioprotective effects against MI/R injury in diabetic rats, which is partly through activation of phosphatidylinositol 3-kinase (PI3 K)/Akt pathway. Thus this study shows a novel pharmacological preconditioning with Ginsenoside Rb1 in the diabetic myocardium.
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Protective effect of Ginsenoside Rb1 against myocardial ischemia/reperfusion injury in streptozotocin-induced diabetic rats
Molecular Biology Reports, 2010Co-Authors: Yang Wu, Li Zhang, Jinjin Xu, Bo ZhaoAbstract:The objective of the current study is to investigate whether Ginsenoside Rb1, a major pharmacological extract of ginseng that could attenuate myocardial ischemia reperfusion (MI/R) injury in non-diabetic myocardium, can attenuate MI/R injury in diabetes that are more vulnerable to ischemic insult. Rats were divided into seven groups: (i) diabetic sham, (ii) diabetic, (iii) normal, (iv) diabetic + Ginsenoside Rb1, (v) diabetic + wortmannin, (vi) diabetic + wortmannin + Ginsenoside Rb1, (vii) diabetic sham + wortmannin. Ginsenoside Rb1 and/or wortmannin were administered prior to inducing MI/R (30 min of coronary artery occlusion followed by 120 min reperfusion). At the end of the experiment, postischemic myocardial infarct size was significantly higher in the diabetic untreated group as compared to normal (P < 0.05), accompanied with increased myocardial apoptosis, elevated plasma CK-MB and LDH release and reduced blood pressure. Ginsenoside Rb1 reduced infarct size, cardiomyocyte apoptosis and caspase-3 activity compared to the diabetic group. The cardioprotective effects of Ginsenoside Rb1 were cancelled by wortmannin. Ginsenoside Rb1 significantly upregulated phosphorylated Akt expression, which was attenuated by wortmannin. Ginsenoside Rb1 exerts cardioprotective effects against MI/R injury in diabetic rats, which is partly through activation of phosphatidylinositol 3-kinase (PI3 K)/Akt pathway. Thus this study shows a novel pharmacological preconditioning with Ginsenoside Rb1 in the diabetic myocardium.
Yang Wu - One of the best experts on this subject based on the ideXlab platform.
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Ginsenoside Rb1 preconditioning enhances enos expression and attenuates myocardial ischemia reperfusion injury in diabetic rats
BioMed Research International, 2011Co-Authors: Bo Zhao, Yang Wu, Li Zhang, Jinjin XuAbstract:Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
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Ginsenoside Rb1 Preconditioning Enhances eNOS Expression and Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats
BioMed Research International, 2011Co-Authors: Bo Zhao, Yang Wu, Li Zhang, Jinjin XuAbstract:Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
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protective effect of Ginsenoside Rb1 against myocardial ischemia reperfusion injury in streptozotocin induced diabetic rats
Molecular Biology Reports, 2011Co-Authors: Yang Wu, Li Zhang, Jinjin Xu, Bo ZhaoAbstract:The objective of the current study is to investigate whether Ginsenoside Rb1, a major pharmacological extract of ginseng that could attenuate myocardial ischemia reperfusion (MI/R) injury in non-diabetic myocardium, can attenuate MI/R injury in diabetes that are more vulnerable to ischemic insult. Rats were divided into seven groups: (i) diabetic sham, (ii) diabetic, (iii) normal, (iv) diabetic + Ginsenoside Rb1, (v) diabetic + wortmannin, (vi) diabetic + wortmannin + Ginsenoside Rb1, (vii) diabetic sham + wortmannin. Ginsenoside Rb1 and/or wortmannin were administered prior to inducing MI/R (30 min of coronary artery occlusion followed by 120 min reperfusion). At the end of the experiment, postischemic myocardial infarct size was significantly higher in the diabetic untreated group as compared to normal (P < 0.05), accompanied with increased myocardial apoptosis, elevated plasma CK-MB and LDH release and reduced blood pressure. Ginsenoside Rb1 reduced infarct size, cardiomyocyte apoptosis and caspase-3 activity compared to the diabetic group. The cardioprotective effects of Ginsenoside Rb1 were cancelled by wortmannin. Ginsenoside Rb1 significantly upregulated phosphorylated Akt expression, which was attenuated by wortmannin. Ginsenoside Rb1 exerts cardioprotective effects against MI/R injury in diabetic rats, which is partly through activation of phosphatidylinositol 3-kinase (PI3 K)/Akt pathway. Thus this study shows a novel pharmacological preconditioning with Ginsenoside Rb1 in the diabetic myocardium.
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Protective effect of Ginsenoside Rb1 against myocardial ischemia/reperfusion injury in streptozotocin-induced diabetic rats
Molecular Biology Reports, 2010Co-Authors: Yang Wu, Li Zhang, Jinjin Xu, Bo ZhaoAbstract:The objective of the current study is to investigate whether Ginsenoside Rb1, a major pharmacological extract of ginseng that could attenuate myocardial ischemia reperfusion (MI/R) injury in non-diabetic myocardium, can attenuate MI/R injury in diabetes that are more vulnerable to ischemic insult. Rats were divided into seven groups: (i) diabetic sham, (ii) diabetic, (iii) normal, (iv) diabetic + Ginsenoside Rb1, (v) diabetic + wortmannin, (vi) diabetic + wortmannin + Ginsenoside Rb1, (vii) diabetic sham + wortmannin. Ginsenoside Rb1 and/or wortmannin were administered prior to inducing MI/R (30 min of coronary artery occlusion followed by 120 min reperfusion). At the end of the experiment, postischemic myocardial infarct size was significantly higher in the diabetic untreated group as compared to normal (P < 0.05), accompanied with increased myocardial apoptosis, elevated plasma CK-MB and LDH release and reduced blood pressure. Ginsenoside Rb1 reduced infarct size, cardiomyocyte apoptosis and caspase-3 activity compared to the diabetic group. The cardioprotective effects of Ginsenoside Rb1 were cancelled by wortmannin. Ginsenoside Rb1 significantly upregulated phosphorylated Akt expression, which was attenuated by wortmannin. Ginsenoside Rb1 exerts cardioprotective effects against MI/R injury in diabetic rats, which is partly through activation of phosphatidylinositol 3-kinase (PI3 K)/Akt pathway. Thus this study shows a novel pharmacological preconditioning with Ginsenoside Rb1 in the diabetic myocardium.