Myocardial infarct is markedly diminished by pretreatment with Genistin, particularly at the high dose. After 1 h of reperfusion, preconditioning with Genistin at dosages of 20 to 60 mg/kg significantly attenuats the release of lactate dehydrogenase (LDH), creatine kinase (CK) in a dose-dependent manner compare with the I/R group. Results show that the level of malondialdehyde (MDA) is decreased and the activities of superoxide dismutase (SOD) and catalase (CAT) are increased as well as an increased glutathione (GSH) level in a dose-dependent manner by Genistin treatment in I/R. Pretreatment with Genistin (20, 40 and 60 mg/kg) also prevents the expression of P2X7, p-IκBα, and p-NF-κB p65 compare with the model group[2].
In Vitro
Genistin is the major isoflavonoid of soybeans and soy products. Genistin shows a dose-dependent superoxide scavenging effect and exhibits major effect at 200 μM, corresponding in activity to 0.08 U/mg protein superoxide dismutase (SOD). Results demonstrate that Genistin exhibits a significantly (P<0.01) and a dose-dependent inhibitory effect on the human cancer cell examined, and at higher concentration (100 μM), the cell viability is 59%. Genistin also induces a significant and dose-dependent increase in ROS formation when compare with the untreated control[1].
Kinase Assay
Cell Assay
Animal Administration
References
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