The Effect of Garlic Oil on Nitric Oxide Production in Coronary Artery Endothelial Cells
Location
Georgia
Start Date
16-5-2017 1:00 PM
Description
INTRODUCTION: Diabetes is an increasing health problem, with cardiovascular disease (CVD) responsible for 75% of diabetic deaths. Unfortunately, there is very little that can be done to reverse CVD in diabetes. Oxidative stress increases in diabetes, yet the mechanisms are unclear. Recent studies indicate that diabetes depletes tetrahydrobiopterin (BH4), a cofactor critical for normal endothelial nitric oxide synthase (eNOS) function. Because garlic has been proposed to preserve BH4, we tested the ability of garlic to reverse oxidative stress in human vascular endothelial cells.
OBJECTIVES: The primary objective of the study was to investigate garlic’s ability to increase NO bioavailability in order to prevent the development of cardiovascular disease in diabetes, and improve overall health of patients.
METHODS: Healthy human coronary artery endothelial cells (HCAEC), and Type I Diabetic (DHCAEC-I), and Type II Diabetic (DHCAEC-II) cells were used. Production of NO and SO before and after garlic oil treatment was detected using fluorescence microscopy, 4-amino-5-methylamino-2’, 7-difluorescein (DAF-FM; 2μM) for NO detection, and dihydroethidium (DHE; 20μM) for SO detection. Protein samples were isolated for immunoblot analysis in control and garlic-exposed endothelial cells.
RESULTS: Garlic oil significantly increased DAF fluorescence compared to baseline in DHCAEC-I, DHCAEC-II, and HCAEC (p<0.0001), and reversed diabetes-induced NO depletion. Control oil vehicle had no effect on NO production. 24-hour exposure to garlic oil decreased eNOS expression significantly in the diabetic cells- 97.25% decrease in DHCAEC-II (p<0.0001) and 82.4% decrease in DHCAEC-I (p<0.01).
CONCLUSION: Enhanced garlic consumption could be a novel, natural mechanism for decreasing eNOS uncoupling and helping to decrease the risk of cardiovascular dysfunction by restoring and/or preserving normal vascular endothelial cell function in both the diabetic and normal states.
Embargo Period
6-20-2017
The Effect of Garlic Oil on Nitric Oxide Production in Coronary Artery Endothelial Cells
Georgia
INTRODUCTION: Diabetes is an increasing health problem, with cardiovascular disease (CVD) responsible for 75% of diabetic deaths. Unfortunately, there is very little that can be done to reverse CVD in diabetes. Oxidative stress increases in diabetes, yet the mechanisms are unclear. Recent studies indicate that diabetes depletes tetrahydrobiopterin (BH4), a cofactor critical for normal endothelial nitric oxide synthase (eNOS) function. Because garlic has been proposed to preserve BH4, we tested the ability of garlic to reverse oxidative stress in human vascular endothelial cells.
OBJECTIVES: The primary objective of the study was to investigate garlic’s ability to increase NO bioavailability in order to prevent the development of cardiovascular disease in diabetes, and improve overall health of patients.
METHODS: Healthy human coronary artery endothelial cells (HCAEC), and Type I Diabetic (DHCAEC-I), and Type II Diabetic (DHCAEC-II) cells were used. Production of NO and SO before and after garlic oil treatment was detected using fluorescence microscopy, 4-amino-5-methylamino-2’, 7-difluorescein (DAF-FM; 2μM) for NO detection, and dihydroethidium (DHE; 20μM) for SO detection. Protein samples were isolated for immunoblot analysis in control and garlic-exposed endothelial cells.
RESULTS: Garlic oil significantly increased DAF fluorescence compared to baseline in DHCAEC-I, DHCAEC-II, and HCAEC (p<0.0001), and reversed diabetes-induced NO depletion. Control oil vehicle had no effect on NO production. 24-hour exposure to garlic oil decreased eNOS expression significantly in the diabetic cells- 97.25% decrease in DHCAEC-II (p<0.0001) and 82.4% decrease in DHCAEC-I (p<0.01).
CONCLUSION: Enhanced garlic consumption could be a novel, natural mechanism for decreasing eNOS uncoupling and helping to decrease the risk of cardiovascular dysfunction by restoring and/or preserving normal vascular endothelial cell function in both the diabetic and normal states.