Difference between revisions of "Team:UST Beijing/Background"
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<h1><span>Cholesterol</span></h1> | <h1><span>Cholesterol</span></h1> | ||
| − | <p>an essential component of membrane structure,gradually | + | <p>an essential component of membrane structure, but gradually |
| − | + | accumulates in arteries of human body, which results in | |
the number one killer mechanism of human life:</p> | the number one killer mechanism of human life:</p> | ||
<p><span>atherosclerosis</span></p> | <p><span>atherosclerosis</span></p> | ||
| − | + | <h1><span> An alarming health threat: Atherosclerosis</span></h1> | |
| − | <h1><span>Atherosclerosis</span></h1> | + | |
<p>Here are the cholesterol structure and pie chart of Epidemic statisitcs of atherosclerosis-related mortality in China</p> | <p>Here are the cholesterol structure and pie chart of Epidemic statisitcs of atherosclerosis-related mortality in China</p> | ||
</blockquote> | </blockquote> | ||
Revision as of 00:47, 11 October 2018
Cholesterol
an essential component of membrane structure, but gradually accumulates in arteries of human body, which results in the number one killer mechanism of human life:
atherosclerosis
An alarming health threat: Atherosclerosis
Here are the cholesterol structure and pie chart of Epidemic statisitcs of atherosclerosis-related mortality in China
Pathology of Atheroscleosis
Artery atherosclerosis refers to arteries accumulated with cholesterol resulting in blockage of blood flow. Cholesterol is the main culprit of cardio-cerebrovascular disease. In heart it results in heart attack. In brain it results in blockage stroke.
Molecular Mechanism of Atherosclerosis Formation
Because of cells’ apoptosis caused by foam cell, which is reversed from macrophages overloading cholesterol, the deposition of cholesterol is formed.
Nuclear receptor LXR as therapeutic target against atherosclerosis
Live X receptor(LXR) functions as a significant regulation switch, which can accelerate the transport of cholesterol and prevent the formation of foam cells.
Ginseng sapogenin’s structure is similar to that of cholesterol, that is to say, it has the potential of regulating LXRs. LXRs has a typical nuclear receptor structure. In the existence of coactivators, regulated by agonists (such as ginsenoside), LXRs could combine the special site in gene promoter region to repress or active the transcripstion of the target gene. So to sum up, ginsenoside could regulate the metabolism of cholesterol. We devote to finding a better way to solve the two remaining problems. Here is the foothold of our project postulates.
Ginsenoside TR1 modulates
LXR biological activity
