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To determine the effects of Ginsenosides Rb3 and PPAR pathway on H9C2 cell injury induced by myocardial ischemia.
Screening of various Ginsenosides Rb3 concentration protection option in H9C2 cell. Then establish the cell model of glucose deprioation/rehabilitation of sugar-oxygen. H9C2 cardiomyoctyes were randomly divided into control groups, model group, Ginsenoside Rb3 groups (0.1umol/L0.5umol/L1umol/L). The expression of transcription factors and key molecules were measured by reverse transcriptase pdymerase chain reaction or western blotting.
The model groups in H9C2 were demonstrated by increasing the expression of NF-KB genes. Ginsenosides Rb3 groups were demonstrated by activating the PPARr and RXR, attenuating the expression of NF-kb genes increasing relative cell viability.
Pretreating with Ginsenosides Rb3 could prevent the H9C2 cells injury induced by myocardial ischemia. The mechanisms may be the activated PPARr suprarin NF-Kb, which attenuates inflammation damages.