Combinational Effects of Apocynin and Mitoquinone in Reducing Myocardial Ischemia/reperfusion (MI/R) Injury
Location
Philadelphia Camppus
Start Date
7-5-2014 1:00 PM
Description
Reactive oxygen species (ROS) is generated due to the influx of oxygen during MI/R and contributes to post-reperfused cardiac contractile dysfunction and increased infarct size. Damaged mitochondria and NADPH oxidase activation are major sites of ROS in MI/R. In prior studies, apo, a NADPH oxidase inhibitor, and mitoQ, a mitochondrial-targeted antioxidant, dose-dependently improved post-reperfused left ventricular developed pressure (LVDP) and reduced infarct size in rat hearts subjected to I(30min)/R(45min). This led us to question whether low doses of apo and mitoQ given together can act synergistically to improve post-reperfused LVDP and reduce infarct size compared to either drug alone or control? Early data shows that the combination of apo (40μM) + mitoQ (1 μM ) (n=7) reduced infarct size to 27 ± 11% compared to mitoQ (1 μM) (n= 6) 54 ± 6% (p
Combinational Effects of Apocynin and Mitoquinone in Reducing Myocardial Ischemia/reperfusion (MI/R) Injury
Philadelphia Camppus
Reactive oxygen species (ROS) is generated due to the influx of oxygen during MI/R and contributes to post-reperfused cardiac contractile dysfunction and increased infarct size. Damaged mitochondria and NADPH oxidase activation are major sites of ROS in MI/R. In prior studies, apo, a NADPH oxidase inhibitor, and mitoQ, a mitochondrial-targeted antioxidant, dose-dependently improved post-reperfused left ventricular developed pressure (LVDP) and reduced infarct size in rat hearts subjected to I(30min)/R(45min). This led us to question whether low doses of apo and mitoQ given together can act synergistically to improve post-reperfused LVDP and reduce infarct size compared to either drug alone or control? Early data shows that the combination of apo (40μM) + mitoQ (1 μM ) (n=7) reduced infarct size to 27 ± 11% compared to mitoQ (1 μM) (n= 6) 54 ± 6% (p