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Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
Published on: April 6, 2017
Chromium picolinate inhibits cholesterol-induced stimulation of platelet aggregation in hypercholesterolemic rats
1Physiology Department, Faculty of Medicine, Ain Shams University, Abbassyia District of Cairo Governorate, on Ahmed Lotfy Al-Sayed Street, Cairo, Egypt, ansamseif@yahoo.com.
Insights
Chromium supplementation normalized high-fat diet-induced increases in plasma lipids and platelet aggregation in rats. This suggests chromium may help manage cardiovascular risk factors associated with hypercholesterolemia.
Area of Science:
- Biochemistry
- Cardiovascular Research
- Nutritional Science
Background:
- Hypercholesterolemia is linked to increased myocardial infarction risk via enhanced platelet aggregation.
- Chromium supplementation is known to potentially reduce plasma lipid levels.
Purpose of the Study:
- To investigate the inhibitory effect of chromium on platelet aggregation in hypercholesterolemic conditions.
- To assess chromium's impact on lipid profiles and platelet activity.
Main Methods:
- Albino rats were divided into control, chromium-supplemented, high-fat diet, and high-fat diet with chromium groups.
- Evaluated adenosine diphosphate and collagen-induced platelet aggregation.
- Measured plasma lipids (cholesterol, triglycerides) and biomarkers (apolipoproteins, thromboxane B2).
Main Results:
- High-fat diet significantly elevated plasma lipids and platelet aggregation.
- Chromium supplementation normalized these elevations in hypercholesterolemic rats.
- Chromium had no significant effect on lipid or platelet activity in normolipemic rats.
Conclusions:
- Chromium supplementation improves lipid profiles in hypercholesterolemic rats.
- It effectively reduces platelet hyperaggregability to normal levels.
- The primary mechanism appears to be a reduction in plasma cholesterol.
Background:
Hypercholesterolemia indirectly increases the risk of myocardial infarction by enhancing platelet aggregation. Chromium has been shown to lower plasma lipids.
Aim:
This study was designed to investigate whether chromium inhibits platelet aggregation under hypercholesterolemic conditions.
Methods:
Albino rats were divided into four groups: control rats fed with a normolipemic diet (NLD group), chromium-supplemented rats fed with NLD (NLD + Cr group), rats fed with a high-fat diet (HF group), and chromium-supplemented rats fed with HF (HF + Cr group). After 10 weeks, blood was collected to determine adenosine diphosphate and collagen-induced platelet aggregation and plasma levels of total cholesterol, triglycerides, high-density lipoprotein cholesterol, apolipoprotein A1, apolipoprotein B, and thromboxane B2. Low-density lipoprotein cholesterol was calculated by Friedewald formula.
Results:
High-fat diet animals displayed significant elevation of plasma lipids and platelet aggregation which was normalized to control levels by chromium supplementation. Chromium supplementation in normolipemic (NLD + Cr) rats did not produce significant changes in either plasma lipids or platelet activity.
Conclusion:
Chromium supplementation to hypercholesterolemic rats improves the lipid profile and returns platelet hyperaggregability to control levels. This normalization is mostly due to a reduction in plasma cholesterol level.
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