Pretreatment with Panaxatriol Saponin Attenuates Mitochondrial Apoptosis and Oxidative Stress to Facilitate Treatment of Myocardial Ischemia-Reperfusion Injury via the Regulation of Keap1/Nrf2 Activity

<div>PTS attenuates H<sub>2</sub>O<sub>2</sub>-induced cardiomyocyte apoptosis depending on the regulation of Nrf2 activity. ML385, a direct activator of the Keap1 and Nrf2 interaction, was used to cotreat H9c2 with vehicle or PTS. (a) Western blotting results showed the changes in apoptosis-related proteins in H9c2 cells after Nrf-2 blockade. (b–e) The levels of cleaved caspase-3, cleaved PRAR-1, Bax, and Cyt-c were quantified using ImageJ. 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Oxidative Medicine and Cellular Longevity

fig5

Figure 5

Figure 5: Pretreatment with Panaxatriol Saponin Attenuates Mitochondrial Apoptosis and Oxidative Stress to Facilitate Treatment of Myocardial Ischemia-Reperfusion Injury via the Regulation of Keap1/Nrf2 Activity 

Figure 5 | Pretreatment with Panaxatriol Saponin Attenuates Mitochondrial Apoptosis and Oxidative Stress to Facilitate Treatment of Myocardial Ischemia-Reperfusion Injury via the Regulation of Keap1/Nrf2 Activity 