Suppression of hyperacute and passively transferred experimental autoimmune encephalomyelitis by the anti-oxidant, butylated hydroxyanisole.
Butylated hydroxyanisole (BHA) was used to treat hyperacute, ordinary passive, and hyperacute passive experimental autoimmune encephalomyelitis (EAE) in the Lewis rat. The anti-oxidant, delivered via mini-osmotic pumps, reduced the incidence, severity and mortality in hyperacute EAE and also reduced the incidence, severity and duration of disease in passively induced EAE and hyperacute passive EAE. In all cases, cellular infiltration by both mononuclear and polymorphonuclear leukocytes were significantly reduced in treated rats. BHA appears therefore to act at the effector stage of EAE, reducing cellular infiltration in the brain and spinal cord and minimising clinical signs without blocking sensitisation or activation. This was supported by the finding that spleen cells from BHA-treated donors immunised for hyperacute EAE transferred disease at least as well as cells recovered from untreated donors.
D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002083:Butylated Hydroxyanisole / Q000494:pharmacology*; D002465:Cell Movement / Q000187:drug effects / Q000276:immunology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D005609:Free Radicals / Q000276:immunology; D007116:Immunization, Passive; D007263:Infusions, Parenteral; D008297:Male; D009504:Neutrophils / Q000166:cytology; D051381:Rats; D011917:Rats, Inbred Lew
D000975:Antioxidants; D005609:Free Radicals; D002083:Butylated Hydroxyanisole