Objectives This study aimed to test the protection of puerarin in oxidative stress-induced mitochondrial injury in rat cardiac H9c2 cells.
Methods Rat heart tissue-derived H9c2 cells were used. First, we test if puerarin could modulate the mPTP opening. To detect the mPTP opening, cells were loaded with TMRE and imaged with confocal microscopy. After treatments with puerarin at different concentrations, cells were exposed to 650 µM H2O2 to induce the mPTP opening, and were tested by the MTT assay to detect cell activity. To define the signalling mechanism responsible for the protective effect of puerarin, phosphor-ylation status of SAPK/JNK and p38MAPK were determined with Western blot.
Cardiac H9c2 cells treated with 0.1 µM puerarin showed a significant increase in TMRE fluorescence intensity compared to the control group, indicating that puerarin can prevent oxidant-induced mitochondrial damage.
MTT assay were used to detect cell activity. Compared to the control group, cells treated with puerarin (0.1 µM) showed a significantly increased in absorbance ratio, indicating the cardioprotective effect of puerarin.
The effect of H2O2 on TMRE fluorescence was inhibited by SP600125, implying that the JNK signalling pathways may mediate the action of Puerarin.
Compared to the control group, cells treated with puerarin (0.1 µM) showed a significant decrease in phosphorylation of SAPK/JNK and did not alter the phosphorylated p38MAPK, indicating that JNK mediates the cardioprotective effect of puerarin.
Conclusions Puerarin may restrain oxidative stress-induced injury through inhibit ing JNK phosphorylation.
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