crocin has been researched along with Demyelinating-Diseases* in 2 studies
2 other study(ies) available for crocin and Demyelinating-Diseases
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Effects of Crocin on brain neurotrophins, cognition, balance and pain in toxic-induced demyelination model.
The purpose of this study was to investigate the effects of Crocin on brain neuroterophins, cognition, sensory and motor dysfunction and compare to fingolimod effects in toxic-induced demyelination with Ethidium Bromide EB in female Wistar rats.. Animals were assigned in to 8 groups; Sham, Sham operated (ShOp), EAE, crocin treated, Vehicle, Fingolompd (Fing) and fingolimod + crocin (Cr+Fing). Demyelination was induced by single dose injection of 10 μl of EB 0.1 percent into the fourth ventricle of the brain. Crocin and fingolimod were administered for 21 days, daily, oral gavage. BDNF, NGF1, tail flake latency, balance and behavioral variables were sampled and analyzed by paired t-test and ANOVA test with repeated post hoc measurements.. The results showed that crocin improves all studied factors, but remarkable improvements were observed in dosage of 10 mg/kg. Crocin (10mg/kg) and fingolimod (1mg/kg) significantly improved cognition variables in open field test, sensory and motor nerve conduction velocity, tail flick latency and clinical scores (p less than 005). In addition, applying of crocin co-administered with fingolimod led to significant increases in all assessed factors, greater than crocin or fingolimod intervention alone.. Based on the current findings, crocin can improve the level of brain neurotrophins, exploratory behavior, balance and pain after toxin-demyelination as close as fingolimod results. Topics: Animals; Brain; Cognition; Demyelinating Diseases; Female; Fingolimod Hydrochloride; Nerve Growth Factors; Pain; Rats; Rats, Wistar | 2024 |
Neuroinflammation and endoplasmic reticulum stress are coregulated by crocin to prevent demyelination and neurodegeneration.
Endoplasmic reticulum (ER) stress is a homeostatic mechanism, which is used by cells to adapt to intercellular and intracellular changes. Moreover, ER stress is closely linked to inflammatory pathways. We hypothesized that ER stress is an integral component of neuroinflammation and contributes to the development of neurological diseases. In autopsied brain specimens from multiple sclerosis (MS) and non-MS patients, XBP-1 spliced variant (XBP-1/s) was increased in MS brains (p < 0.05) and was correlated with the expression of the human endogenous retrovirus-W envelope transcript, which encodes the glycoprotein, Syncytin-1 (p < 0.05). In primary human fetal astrocytes transfected with a Syncytin-1-expressing plasmid, XBP-1/s, BiP, and NOS2 were induced, which was suppressed by crocin treatment (p < 0.05). Crocin also protected oligodendrocytes exposed to cytotoxic supernatants derived from Syncytin-1-expressing astrocytes (p < 0.05) and NO-mediated oligodendrocytotoxicity (p < 0.05). During experimental autoimmune encephalomyelitis (EAE), the transcript levels of the ER stress genes XBP-1/s, BiP, PERK, and CHOP were increased in diseased spinal cords compared with healthy littermates (p < 0.05), although CHOP expression was not involved in the EAE disease phenotype. Daily treatment with crocin starting on day 7 post-EAE induction suppressed ER stress and inflammatory gene expression in spinal cords (p < 0.05), which was accompanied by preserved myelination and axonal density, together with reduced T cell infiltration and macrophage activation. EAE-associated neurobehavioral deficits were also ameliorated by crocin treatment (p < 0.05). These findings underscored the convergent roles of pathogenic ER stress and immune pathways in neuroinflammatory disease and point to potential therapeutic applications for crocin. Topics: Animals; Carotenoids; Cells, Cultured; Demyelinating Diseases; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental; Endoplasmic Reticulum; Female; Free Radical Scavengers; Frontal Lobe; Humans; Inflammation Mediators; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Middle Aged; Neurodegenerative Diseases; Rats; Rats, Sprague-Dawley | 2011 |