stigmasterol/slagtilfælde

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Lymphatic absorption and deposition of various plant sterols in stroke-prone spontaneously hypertensive rats, a strain having a mutation in ATP binding cassette transporter G5.

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ATP binding cassette transporter G5 (ABCG5) and ATP binding cassette transporter G8 (ABCG8) have been suggested to transport absorbed plant sterols and cholesterol from enterocytes to the intestinal lumen and from hepatocytes to bile. It has been thought that mutations of ABCG5 or ABCG8 cause the

Stigmasterol stimulates transintestinal cholesterol excretion independent of liver X receptor activation in the small intestine.

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Despite advances in healthcare, cardiovascular disease (CVD) remains the leading cause of death in the United States. Elevated levels of plasma cholesterol are highly predictive of CVD and stroke and are the principal driver of atherosclerosis. Unfortunately, current cholesterol lowering agents,

Stigmasterol Exerts Neuro-Protective Effect Against Ischemic/Reperfusion Injury Through Reduction Of Oxidative Stress And Inactivation Of Autophagy.

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Stroke remains the primary cause of pain, suffering, and death in patients. One of the major thrusts in stroke therapy is to find an effective prevention strategy. Objectives of this study are to testify the neuro-protection effect of stigmasterol in ischemic/reperfusion injury

Missense mutation in Abcg5 in SHRSP rats does not accelerate intestinal absorption of plant sterols: comparison with Wistar rats.

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Stroke-prone spontaneously hypertensive rats (SHRSP) deposit plant sterols in their bodies and have a mutation in ATP binding cassette transporter G5 (Abcg5). Lymphatic recovery rates of campesterol and sitosterol in SHRSP rats were comparable to those in Wistar rats, a strain that does not deposit

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