Title

INHIBITION OF STROKE-INDUCED ACTIVITY OF THE APOPTOTIC ENZYME CASPASE-3

Presentation Type

Poster

Abstract

Stroke is the leading cause of adult disability in the United States. Ischemic stroke, the most common type, occurs when a blood vessel in the brain is blocked, depriving the affected area of oxygen and glucose, causing cell death and tissue damage. Stroke also involves delayed programmed cell death, called apoptosis, which causes further neuronal damage. The enzyme caspase-3 plays a significant role in this apoptotic process. Through inhibition of caspase-3, apoptotic-mediated tissue damage may be reduced. The unique compound PM12-18H, which was isolated from a fungus found in the Berkeley Pit (Butte, MT, USA), was selected for examination based on its ability to inhibit caspase-3. In the current study, we evaluated this compound’s potential to mitigate the damaging effects of stroke. The primary goals were to determine its effectiveness as a caspase-3 inhibitor and its ability to inhibit apoptosis. A mouse neuroblastoma cell line, N2A, was subjected to oxygen and glucose deprivation for sixty minutes to simulate severe stroke-like conditions. Afterward, the cells underwent a four-hour simulated reperfusion period with oxygen and glucose in the presence of PM12-18H. To measure the effect of this compound, a caspase-3 activity assay (ApoAlert) was performed. Treatment with PM12-18H resulted in significant inhibition of caspase-3 compared to a control. In conclusion, PM12-18H can inhibit caspase-3 and future research will uncover its potential to inhibit apoptosis in stroke, ultimately leading to further investigation of caspase-3 inhibitors as a therapeutic target for stroke patients.

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Apr 15th, 11:00 AM Apr 15th, 12:00 PM

INHIBITION OF STROKE-INDUCED ACTIVITY OF THE APOPTOTIC ENZYME CASPASE-3

UC South Ballroom

Stroke is the leading cause of adult disability in the United States. Ischemic stroke, the most common type, occurs when a blood vessel in the brain is blocked, depriving the affected area of oxygen and glucose, causing cell death and tissue damage. Stroke also involves delayed programmed cell death, called apoptosis, which causes further neuronal damage. The enzyme caspase-3 plays a significant role in this apoptotic process. Through inhibition of caspase-3, apoptotic-mediated tissue damage may be reduced. The unique compound PM12-18H, which was isolated from a fungus found in the Berkeley Pit (Butte, MT, USA), was selected for examination based on its ability to inhibit caspase-3. In the current study, we evaluated this compound’s potential to mitigate the damaging effects of stroke. The primary goals were to determine its effectiveness as a caspase-3 inhibitor and its ability to inhibit apoptosis. A mouse neuroblastoma cell line, N2A, was subjected to oxygen and glucose deprivation for sixty minutes to simulate severe stroke-like conditions. Afterward, the cells underwent a four-hour simulated reperfusion period with oxygen and glucose in the presence of PM12-18H. To measure the effect of this compound, a caspase-3 activity assay (ApoAlert) was performed. Treatment with PM12-18H resulted in significant inhibition of caspase-3 compared to a control. In conclusion, PM12-18H can inhibit caspase-3 and future research will uncover its potential to inhibit apoptosis in stroke, ultimately leading to further investigation of caspase-3 inhibitors as a therapeutic target for stroke patients.