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Advanced Glycation Endproducts Are Increased in the Animal Model of Multiple Sclerosis but Cannot Be Reduced by Pyridoxamine Treatment or Glyoxalase 1 Overexpression
- Source :
- International Journal of Molecular Sciences, Vol 19, Iss 5, p 1311 (2018), International Journal of Molecular Sciences; Volume 19; Issue 5; Pages: 1311, International journal of molecular sciences, 19(5):1311. Multidisciplinary Digital Publishing Institute (MDPI), International Journal of Molecular Sciences
- Publication Year :
- 2018
-
Abstract
- Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system (CNS). The immune response in MS patients leads to the infiltration of immune cells in the CNS and their subsequent activation. Immune cell activation induces a switch towards glycolysis. During glycolysis, the dicarbonyl product methylglyoxal (MGO) is produced. MGO is a glycating agent that can rapidly form advanced glycation endproducts (AGEs). In turn, AGEs are able to induce inflammatory responses. The glyoxalase system is the endogenous defense system of the body to reduce the burden of MGO thereby reducing AGE formation. This system consists of glyoxalase-1 and glyoxalase-2 which are able to detoxify MGO to D-lactate. We investigated whether AGE levels are induced in experimental autoimmune encephalitis (EAE), an inflammatory animal model of MS. Twenty seven days post EAE induction, MGO and AGE (Nε-(carboxymethyl)lysine (CML), Nε-(carboxyethyl)lysine (CEL), 5-hydro-5-methylimidazolone (MG-H1)) levels were significantly increased in the spinal cord of mice subjected to EAE. Yet, pyridoxamine treatment and glyoxalase-1 overexpression were unable to counteract AGE production during EAE and did not influence the clinical course of EAE. In conclusion, AGEs levels increase during EAE in the spinal cord, but AGE-modifying treatments do not inhibit EAE-induced AGE production and do not affect disease progression.
- Subjects :
- Glycation End Products, Advanced
0301 basic medicine
END-PRODUCTS AGES
experimental autoimmune encephalomyelitis
multiple sclerosis
DISEASE
lcsh:Chemistry
chemistry.chemical_compound
0302 clinical medicine
advanced glycation endproducts
pyridoxamine
glyoxalase-1
Medicine
lcsh:QH301-705.5
Spectroscopy
INSULIN-RESISTANCE
PLASMA
Methylglyoxal
Experimental autoimmune encephalomyelitis
Lactoylglutathione Lyase
Brain
General Medicine
Pyruvaldehyde
Computer Science Applications
medicine.anatomical_structure
Spinal Cord
METHYLGLYOXAL
Vitamin B Complex
Female
Glycolysis
medicine.medical_specialty
Encephalomyelitis, Autoimmune, Experimental
Central nervous system
METABOLISM
Article
Catalysis
Inorganic Chemistry
03 medical and health sciences
Immune system
CEREBROSPINAL-FLUID
Internal medicine
Animals
Humans
Physical and Theoretical Chemistry
Molecular Biology
Autoimmune disease
business.industry
Multiple sclerosis
Organic Chemistry
medicine.disease
Mice, Inbred C57BL
MICE
030104 developmental biology
Endocrinology
lcsh:Biology (General)
lcsh:QD1-999
chemistry
Pyridoxamine
business
030217 neurology & neurosurgery
SYSTEM
Glyoxalase system
Subjects
Details
- Language :
- English
- ISSN :
- 14220067
- Volume :
- 19
- Issue :
- 5
- Database :
- OpenAIRE
- Journal :
- International journal of molecular sciences
- Accession number :
- edsair.doi.dedup.....4f88225844fdee3dab7bfe749fe5ef9a