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Names | |
---|---|
IUPAC name
(24S)-Cholest-5-ene-3β,24-diol
| |
Systematic 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
| |
Identifiers | |
3D model (
JSmol)
|
|
3218472 | |
ChEBI | |
ChEMBL | |
ChemSpider | |
KEGG | |
PubChem
CID
|
|
UNII | |
CompTox Dashboard (
EPA)
|
|
| |
| |
Properties | |
C27H46O2 | |
Molar mass | 402.663 g·mol−1 |
Except where otherwise noted, data are given for materials in their
standard state (at 25 °C [77 °F], 100 kPa).
|
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] as well as acting as a positive allosteric modulator of NMDA receptors. [9] 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. [10] Blood plasma levels of 24S-HC may be altered after acute brain injuries such as stroke [11] or in neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and multiple sclerosis. [12] [13]
![]() | |
Names | |
---|---|
IUPAC name
(24S)-Cholest-5-ene-3β,24-diol
| |
Systematic 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
| |
Identifiers | |
3D model (
JSmol)
|
|
3218472 | |
ChEBI | |
ChEMBL | |
ChemSpider | |
KEGG | |
PubChem
CID
|
|
UNII | |
CompTox Dashboard (
EPA)
|
|
| |
| |
Properties | |
C27H46O2 | |
Molar mass | 402.663 g·mol−1 |
Except where otherwise noted, data are given for materials in their
standard state (at 25 °C [77 °F], 100 kPa).
|
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] as well as acting as a positive allosteric modulator of NMDA receptors. [9] 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. [10] Blood plasma levels of 24S-HC may be altered after acute brain injuries such as stroke [11] or in neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and multiple sclerosis. [12] [13]