Difference between revisions of "Team:UST Beijing/Background"
| Line 31: | Line 31: | ||
<!--logo--> | <!--logo--> | ||
<button type="button" class="btn btn-navbar" data-toggle="collapse" data-target=".nav-collapse"> <i class="fa fa-bars"></i></button> | <button type="button" class="btn btn-navbar" data-toggle="collapse" data-target=".nav-collapse"> <i class="fa fa-bars"></i></button> | ||
| − | <div class="logo"> <a href=""><img src="https://static.igem.org/mediawiki/2018/9/93/T--UST_Beijing--USTBCUblack.png" width=" | + | <div class="logo"> <a href=""><img src="https://static.igem.org/mediawiki/2018/9/93/T--UST_Beijing--USTBCUblack.png" width="180" height="60" alt="" class="animated bounceInDown" /></a> </div> |
<!--menu--> | <!--menu--> | ||
<nav id="main_menu"> | <nav id="main_menu"> | ||
Revision as of 08:21, 12 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
Shown on the right are the cholesterol structure and pie charts of Epidemic statistics 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 causes heart attack. In brain it causes blockage stroke.
Molecular Mechanism of Atherosclerosis Formation
Because of foam cell apoptosis, which is formed by macrophages overloading cholesterol, cholesterol is deposited on the inner wall of artery.
Nuclear receptor LXR as therapeutic target against atherosclerosis
Live X receptor(LXR) functions as a master regulation switch, which can accelerate the transport of cholesterol and prevent the formation of foam cells.
Ginseng triterpenes' structure is similar to that of cholesterol, that is to say, it has the potential of regulating LXRs. LXRs is a typical nuclear receptor. In the presence of co-activators, regulated by agonists (such as ginsenoside), LXRs could binds special site on target gene promoter region to repress or active the transcription of the target gene. So to sum up, ginsenosides 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
