Names | |
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IUPAC name
Cholest-5-ene-3,24-diol
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Preferred IUPAC name
(1R,3aS,3bS,7S,9aR,9bS,11aR)-1-[(2R,5S)-5-Hydroxy-6-methylheptan-2-yl]-9a,11a-dimethyl-2,3,3a,3b,4,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-7-ol | |
Other names
cerebrosterol
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Identifiers | |
3D model (JSmol)
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3218472 | |
ChEBI | |
ChEMBL | |
ChemSpider | |
KEGG | |
PubChem CID
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UNII | |
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Properties | |
C27H46O2 | |
Molar mass | 402.653 g/mol |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). | |
Infobox references | |
24S-Hydroxycholesterol (24S-HC), also known as cholest-5-ene-3,24-diol or cerebrosterol, is an endogenous oxysterol produced by neurons in the brain to maintain cholesterol homeostasis.[1] It was discovered in 1953 by Alberto Ercoli, S. Di Frisco, and Pietro de Ruggieri, who first isolated the molecule in the horse brain[2] and then demonstrated its presence in the human brain.[3]
24S-HC is produced by a hydroxy group substitution at carbon number 24 in cholesterol, catalyzed by the enzyme cholesterol 24-hydroxylase (CYP46A1).[4]
24S-HC binds to apolipoproteins such as apoE, apoJ, and apoA1 to form HDL-like complexes[5] which can cross the blood-brain barrier more easily than free cholesterol. Thus, 24S-HC production serves as one of several counterbalancing mechanisms for cholesterol synthesis in the brain.[1][6] After entering general blood circulation and traveling to the liver, 24S-HC can be sulfated, glucuronidated, or converted into bile acids, which can ultimately be excreted.[7]
24S-HC is an agonist of liver X receptors, a class of nuclear receptors that sense oxysterols. In the brain, liver X receptor beta is the primary LXR type which interacts with 24S-HC.[5] 24S-HC levels sensed by LXRs can regulate the expression of SREBP mRNA and protein, which in turn regulate cholesterol synthesis and fatty acid synthesis.[8]
24S-HC may participate in several aspects of brain development and function, such as axon and dendrite growth or synaptogenesis.[4] Regulation of 24S-HC metabolism in neurons may play a role in their health and function, as well as their response to injury or disease.[9] Blood plasma levels of 24S-HC may be altered after acute brain injuries such as stroke[10] or in neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and multiple sclerosis.[11][12]