Abstract
Background
The most common non-traumatic neurological disease in young- and middle-aged adults
is multiple sclerosis (MS), leading to central nervous system (CNS) atrophy and neurological
disorders with loss of myelin and axonal degeneration. Due to the inadequate efficiency
of common treatments, some natural products with antioxidant properties such as Carvacrol
have been considered.
Objective
the present study aimed to investigate carvacrol's anti-inflammatory and therapeutic
effects on MS symptoms in healthy and experimental autoimmune encephalomyelitis (EAE)
induced female Lewis rats.
Methods
The study was performed in three groups of Lewis rats: control group, EAE model, and
EAE treated with carvacrol (carvacrol-treated group). The treatment group received
25 mg/kg of carvacrol intraperitoneally daily. Histologic examination and expression
analysis of pro-inflammatory genes (Interleukin-1 and 17 (IL-1 and IL-17), Nuclear
Factor Kappa B Cells (NF-κB) and Tumor Necrosis Factor-α (TNF-α)), myelin repair,
and also regeneration genes (Myelin basic protein (MBP), Oligodendrocyte Transcription
Factor 2 (OLIG2) and Platelet-Derived Growth Factor Receptor α (PDGFR-α)) were carried
out. Gene studies, Hematoxylin and Eosin (H&E), and Luxol fast blue stain were performed
in the lumbar region of the spinal cord.
Results
The EAE clinical scores in the carvacrol-treated group were lower than in untreated
rats (P < 0.001). The expression of two genes, IL-17 and MBP, was confirmed using fluorescence
immunohistochemistry (FIHC). A significant decrease was observed in NF-κB and IL-17,
and IL-1 gene expression. The MBP and OLIG2 gene expression was increased in the carvacrol-treated
group (p < 0.001). In EAE, PDGFR-α expression increased about four times. However, carvacrol
administration did not affect PDGFR-α and TNF-α gene expression. In this treatment,
H&E staining of spinal cord regions showed a significant decrease in inflammatory
cell infiltration. Moreover, immunostaining analysis demonstrated a considerable increase
in MBP and a reduction in IL-17 secretion.
Conclusion
The results showed that carvacrol administration reduces the entry of inflammatory
cells into the CNS by stimulating myelination-related processes employing increasing
the expression of genes involved in myelin repair and reducing the expression of inflammatory
genes. Our findings confirm that carvacrol improves the clinical and pathological
symptoms of EAE through its therapeutic and modification properties as a potential
adjunctive therapy and needs to be studied more.
Keywords
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Article info
Publication history
Published online: December 16, 2022
Accepted:
December 15,
2022
Received:
July 18,
2022
Identification
Copyright
© 2022 Elsevier B.V. All rights reserved.
