Высококалорийный диетический экскасербирует нейроинфламмуацию и болезнетворность в крысиной модели множественного склероза.
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Gheibi Shahsanam, YahyaZadeh Masood, Karimipour Mojtaba, Ghazavi Ahad, Kashfi Khosrow
Аннотация
Оригинал публикации
High-Fat Diet Exacerbates Neuroinflammation and Disease Severity in a Rat Model of Multiple Sclerosis.
BACKGROUND: Multiple sclerosis (MS) is an autoimmune inflammatory disorder of the central nervous system. The use of high-fat diet is a modifiable risk factor for a variety of inflammatory diseases. Thus, the aim of this study was to investigate the effects of a high-fat diet on the progression of MS in a validated animal model.
METHODS: Adult Wistar rats (N = 10/group) were randomly divided into four groups: (1) standard diet, (2) high-fat diet, (3) and (4) standard and high-fat diet for 45 days, followed by induction of experimental encephalomyelitis. Animals were evaluated for clinical symptoms of MS and biochemical tests, including total cholesterol (TC), triglyceride (TG), low- and high-density lipoprotein-cholesterol (LDL-C and HDL-C), fibrinogen, interferon-gamma (IFN-γ), and interleukin-17 (IL-17). Tissue samples were subjected to neuropathological evaluation. The analysis was performed by one-way analysis of variance (ANOVA).
RESULTS: The high-fat diet increased the progression of experimental autoimmune encephalomyelitis (EAE) disease, INF-γ (approximately 1.5 folds), IL-17 levels (approximately 3 folds), lymphocyte proliferation, TG (approximately 40 folds), TC (approximately 80 folds), LDL-C (approximately 14 folds), and fibrinogen levels (approximately 100 folds), but HDL-C (approximately 40 folds) was decreased (P < 0.05) in the affected MS group compared to standard diet.
CONCLUSIONS: This study demonstrates that a high-fat diet significantly worsens clinical and immunological outcomes in an animal model of MS. The elevation of pro-inflammatory cytokines, particularly IFN-γ and IL-17, suggests that dietary fat may promote an inflammatory environment that accelerates disease progression. These findings highlight the need for further research to elucidate the underlying mechanisms.