Eleutheroside D
Eleutheroside has protective effect to myocardial ischemic-reperfusion injury(IRI) in isolated rats.
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Protective Effect of Eleutheroside Preconditioning to Myocardial Ischemic Reperfusion Injury in Isolated Rats[Reference:
WebLink]
To investigate the protective effect of eleutherosid preconditioning to myocardial ischemic-reperfusion injury(IRI) in isolated rats and the dose-effect relationship between eleutheroside preconditioning and the myocardial protection.
METHODS AND RESULTS:
Male rat hearts,which were isolated and perfused with Langendorff apparatus,were randomly divided into 5 groups,6 in each.The isolated hearts were subjected to 25 min ischemia and then followed by 30 min reperfusion after 15min stabilization in control group(C).In the eleutheroside preconditioned groups(P1,P2,P3,P4),the hearts were perfused with eleutheroside(30 mg/kg,40 mg/kg,60 mg/kg and 80mg/kg,respectively) for 10 min before ischemia-reperfusion.Left ventricular developed pressure(LVDP),left ventricular end diastolic pressure(LVEDP),maximal rate of increase /decrease of left ventricular pressure(±dp/d tMax),and coronary blood flow(CF) were monitored continuously.And an arrhythmias score was used to quantify the arrhythmias during reperfusion.After reperfusing 30 min reperfusion,as compared with group C,① P2 and P3 groups might increase LVDP、+dp/dtMax and-dp/dtMax more significantly(P0.05);②P2 and P3 groups might raise CF more significantly(P0.01);③P2 and P3 groups had lower arrhythmia scores(P0.05).
CONCLUSIONS:
Eleutheroside preconditioning has a dose-effect on IRI of isolated rat hearts.
Evid Based Complement Alternat Med . 2013;2013:934183.
Eleutheroside E, An Active Component of Eleutherococcus senticosus, Ameliorates Insulin Resistance in Type 2 Diabetic db/db Mice[Pubmed:
23690865]
Abstract
Eleutheroside E (EE), a principal component of Eleutherococcus senticosus (ES), has anti-inflammatory and protective effects in ischemia heart. However, it is unknown whether it ameliorates insulin resistance and reduces hyperglycemia in diabetes. This study investigated the effect of EE-containing ES extracts, as well as EE, on hyperglycemia and insulin resistance in db/db mice. EE increased the insulin-provoked glucose uptake in C2C12 myotubes. Moreover, EE improved TNF- α -induced suppression of glucose uptake in 3T3-L1 adipocytes. Five-week-old db/db mice were fed a diet consisting of ES extract or EE for 5 weeks. Both were effective in improving serum lipid profiles and significantly decreased blood glucose and serum insulin levels. ES and EE supplementation effectively attenuated HOMA-IR. Glucose tolerance and insulin tolerance tests showed that EE increased insulin sensitivity. Immunohistochemical staining indicated that ES and EE protected pancreatic alpha and beta cells from diabetic damage. In addition, ES and EE improved hepatic glucose metabolism by upregulating glycolysis and downregulating gluconeogenesis in obese type 2 diabetic mice. These data suggest that EE mediates the hyperglycemic effects of ES by regulating insulin signaling and glucose utilization. The beneficial effects of EE may provide an effective and powerful strategy to alleviate diabetes.
