Location
Philadelphia, PA
Start Date
3-5-2023 1:00 PM
End Date
3-5-2023 4:00 PM
Description
Introduction:
Reperfusion to an ischemic myocardium could result in damage termed myocardial ischemia/reperfusion (I/R) injury. Mitochondrial dysfunction is a major factor in I/R injury, producing less ATP and generating more reactive oxygen species (ROS). Mitoquinone (MitoQ) is an antioxidant that highly accumulates in the mitochondria. However, the dose-response effects and underlying mechanisms of MitoQ on simulated I/R injury have not been well established.
Objectives:
We hypothesized that H9c2 myoblast cells would be damaged by simulated I/R. Moreover, MitoQ would attenuate myocardial injury, characterized by increased cell viability, compared to non-treated control.
Methods:
The H9c2 myoblast cells (less than 20 passages) were treated with or without various concentrations of MitoQ (0.005, 0.05, 0.1, 0.5, 1, 2, 5 μM) under 3 different mediums: normal (containing 4.5 g glucose and pyruvate), low glucose (containing 1 g glucose and pyruvate), and no glucose/pyruvate medium. Three different experiments were conducted on the cells. The first experiment aimed to determine if MitoQ alone exerts different effects under different medium conditions by treating the cells with MitoQ for 24 hrs in a normal incubator. The second experiment aimed to determine if MitoQ increased cell viability under simulated ischemia conditions after MitoQ pretreatment. The third experiment aimed to determine if MitoQ increased cell viability under simulated I/R conditions after MitoQ pretreatment. Cell viability was measured by absorbance at 450 nm after adding a cell counting agent. The change in cell viability was expressed as ratios relative to the untreated controls.
Results:
Low concentrations of MitoQ alone slightly increased cell viability in all three mediums. The maximum increased cell viability was 1.25 ± 0.07 (n=9) at 0.005 μM MitoQ in the normal medium, 1.35 ± 0.23 (n=5, p
MitoQ pretreatment exerts protection to cells in simulated ischemia conditions at certain MitoQ concentrations. The maximum increased cell viability was 1.37 ± 0.3 (n=4) at 0.01 μM MitoQ in normal medium, 1.20 ± 0.13 (n=4) at 1.0 μM MitoQ in low glucose medium, and 1.45 ± 0.24 (n=3) at 0.1 μM MitoQ in no glucose medium compared to the untreated control.
MitoQ effects on simulated I/R injury will be reported in the future.
Discussion:
Preliminary data shows the effects of MitoQ alone and MitoQ pretreatment in ischemic conditions on cell viability is influenced by different mediums and concentrations of MitoQ.
Embargo Period
6-7-2023
Included in
The effects of Mitoquinone on simulated ischemia/reperfusion injuries in H9c2 cells
Philadelphia, PA
Introduction:
Reperfusion to an ischemic myocardium could result in damage termed myocardial ischemia/reperfusion (I/R) injury. Mitochondrial dysfunction is a major factor in I/R injury, producing less ATP and generating more reactive oxygen species (ROS). Mitoquinone (MitoQ) is an antioxidant that highly accumulates in the mitochondria. However, the dose-response effects and underlying mechanisms of MitoQ on simulated I/R injury have not been well established.
Objectives:
We hypothesized that H9c2 myoblast cells would be damaged by simulated I/R. Moreover, MitoQ would attenuate myocardial injury, characterized by increased cell viability, compared to non-treated control.
Methods:
The H9c2 myoblast cells (less than 20 passages) were treated with or without various concentrations of MitoQ (0.005, 0.05, 0.1, 0.5, 1, 2, 5 μM) under 3 different mediums: normal (containing 4.5 g glucose and pyruvate), low glucose (containing 1 g glucose and pyruvate), and no glucose/pyruvate medium. Three different experiments were conducted on the cells. The first experiment aimed to determine if MitoQ alone exerts different effects under different medium conditions by treating the cells with MitoQ for 24 hrs in a normal incubator. The second experiment aimed to determine if MitoQ increased cell viability under simulated ischemia conditions after MitoQ pretreatment. The third experiment aimed to determine if MitoQ increased cell viability under simulated I/R conditions after MitoQ pretreatment. Cell viability was measured by absorbance at 450 nm after adding a cell counting agent. The change in cell viability was expressed as ratios relative to the untreated controls.
Results:
Low concentrations of MitoQ alone slightly increased cell viability in all three mediums. The maximum increased cell viability was 1.25 ± 0.07 (n=9) at 0.005 μM MitoQ in the normal medium, 1.35 ± 0.23 (n=5, p
MitoQ pretreatment exerts protection to cells in simulated ischemia conditions at certain MitoQ concentrations. The maximum increased cell viability was 1.37 ± 0.3 (n=4) at 0.01 μM MitoQ in normal medium, 1.20 ± 0.13 (n=4) at 1.0 μM MitoQ in low glucose medium, and 1.45 ± 0.24 (n=3) at 0.1 μM MitoQ in no glucose medium compared to the untreated control.
MitoQ effects on simulated I/R injury will be reported in the future.
Discussion:
Preliminary data shows the effects of MitoQ alone and MitoQ pretreatment in ischemic conditions on cell viability is influenced by different mediums and concentrations of MitoQ.