![]() ![]() The endogenous neurotransmitter, noradrenaline, exerts anti-inflammatory and neuroprotective effects in vivo and in vitro ( 10, 11). Numerous studies have demonstrated that noradrenaline levels are altered in the CNS of patients with multiple sclerosis, and that noradrenaline levels are reduced in the brainstem and spinal cord of rats with EAE ( 5, 8, 9). The LC-selective neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4), ( 6) significantly increases the clinical severity of experimental autoimmune encephalomyelitis (EAE) in mice ( 7), which suggests that the functional status of LC influences EAE disease. The immunized mice additionally exhibited increased astrocyte activation and neuronal damage in the LC ( 5). In mice immunized with myelin oligodendrocyte glycoprotein peptide MOG 35–55, cortical and spinal cord levels of noradrenaline were significantly reduced compared with control mice ( 5). A magnetic resonance study demonstrated an impairment of selective attention in MS, which was increased with axonal damage at the right LC ( 4). Increasing evidence suggests that abnormalities of the locus coeruleus noradrenaline (LC-NA) system may be a contributing factor for myelin damage. Currently, MS is believed to be a complex multifactorial disease, involving genetic and environmental factors affecting the autoimmune responses that damage the myelin ( 3). The etiology and pathogenesis of the disease, however, remain unclear. It affects 0.1% people in the western world and results in chronic disability, primarily in young adults ( 2). Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS), which is characterized by widespread regions of focal demyelination, loss of oligodendrocytes and axonal degeneration ( 1). These results suggested that drugs targeting LC survival and function, including catalpol, may be able to benefit patients with MS. In primary cultures, catalpol exerted a neuroprotective effect in rat LC neurons by increasing the noradrenaline output. Furthermore, catalpol increased TH expression and increased noradrenaline levels in the spinal cord. Significant improvements in the clinical scores were observed in catalpol-treated mice. ![]() The present study used an experimental mouse model of autoimmune encephalomyelitis to verify the neuroprotective effects of catalpol. Catalpol is an iridoid glycoside purified from Rehmannia glutinosa Libosch, which exerts a neuroprotective effect in multiple sclerosis (MS). TH is the rate-limiting enzyme for noradrenaline synthesis therefore, regulation of TH protein expression and intrinsic enzyme activity represents the central means for controlling the synthesis of noradrenaline. The primary source of noradrenaline in the central nervous system is tyrosine hydroxylase (TH)-positive neurons, located in the locus coeruleus (LC). Reduced noradrenaline levels results in increased inflammation and neuronal damage. The endogenous neurotransmitter, noradrenaline, exerts anti-inflammatory and neuroprotective effects in vivo and in vitro. ![]()
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