Experimental autoimmune neuritis (EAN) is a widely used animal model of the human
acute inflammatory demyelinating polyradiculoneuropathy, which is the most common subtype of
Guillain-Barré Syndrome. EAN is pathologically characterized by breakdown of the blood-nerve barrier, infiltration of reactive immune cells, local
inflammation,
demyelination in the peripheral nervous system and
mechanical allodynia.
Minocycline is known to have neuroprotective and anti-inflammatory effects. Furthermore, relieve of
neuropathic pain following
minocycline administration was observed in a variety of animal models. Here, we investigated the effects of
minocycline on rat EAN. Suppressive treatment with
minocycline (50 mg/kg
body weight daily immediately after immunization) significantly attenuated the severity and duration of EAN. Macrophage and T-cell infiltration and
demyelination in sciatic nerves of EAN rats treated with
minocycline were significantly reduced compared to
phosphate-buffered saline (PBS)-treated EAN rats.
mRNA expressions of matrix metallopeptidase-9,
inducible nitric oxide synthase and pro-inflammatory
cytokines interleukin-1 beta and tumour
necrosis factor-alpha in EAN sciatic nerves were greatly decreased by administration of
minocycline as well. Furthermore,
minocycline attenuated
mechanical allodynia in EAN rats and greatly suppressed spinal microglial activation. All together, our data showed that
minocycline could effectively suppress the peripheral and spinal
inflammation (immune activation) to improve outcome in EAN rats, which suggests that
minocycline may be considered as a potential candidate of pharmacological treatment for autoimmune-mediated neuropathies.