Eleutheroside E (EE), a principal component of Eleutherococcus senticosus (ES), has anti-inflammatory and protective effects in ischemia heart. EE increased the insulin-provoked glucose uptake in C2C12 myotubes. Moreover, EE improved TNF- α -induced suppression of glucose uptake in 3T3-L1 adipocytes. EE mediates the hyperglycemic effects of ES by regulating insulin signaling and glucose utilization[3]. The IC50 values for EB and EE were calculated to be 193.20 μM and 188.36 μM for CYP2E1, 595.66 μM and 261.82 μM for CYP2C9, respectively[4]. EE administration attenuated the cardiomyocyte apoptosis induced by hypoxia-reoxygenation (H/R) injury. Further, pre-treatment with EE dramatically inhibited mitochondrial oxidative stress, IκBα phosphorylation and nuclear factor kappa B (NF-κB) subunit p65 translocation into nuclei. EE might suppress the MAPK signaling pathway to inhibit the H/R-induced NF-κB activation. EE may be a potential drug for myocardial I/R injury by reducing oxidative stress, NF-κB activation, and metabolic reprogramming[5].
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