Elevated interleukin-1β serum level after chronic peripheral salsolinol administration

The catechol isoquinoline derivatives are endogenous compounds present in the mammalian brain and the representative one is referred to as salsolinol. It may be formed from aromatic amines leading to neurotoxic N-methyltetrahydroquinolinium ions that may play a role in the etiology of Parkinson's disease (PD). Neuroinflammation and apoptosis is thought to be a major contributor to the neuronal degeneration in PD. The alteration of inflammatory cytokines in the brain, cerebral spinal fluid and plasma of PD patients supports the existence of functional interconnections between the immune and nervous systems. In animal studies, chronic administration of salsolinol induced parkinsonian-like symptoms, both peripherally and centrally. However, still little has been known about the effects of salsolinol on the pro-inflammatory cytokine production or mast cells activation in the gastrointestinal tract. Male Wistar rats were subjected to continuous intraperitoneal dosing of salsolinol (200 mg/kg in total) with osmotic mini-pumps for two or four weeks and fed with either standard or high fat diet. An equivalent group of rats served as the appropriate controls. At the end of the experiment animals were decapitated and blood samples as well as tissue fragments were collected. Serum samples were assayed immunoenzymatically for IL-11β and by liquid chromatography-mass spectrometry for histamine. Tissue fragments from gastric antrum, duodenum and proximal colon were formalin fixed, paraffin-embedded and stained with either hematoxylin and eosin or toluidine blue. Once activated, mast cells might secrete a range of neurosensitizing and pro-inflammatory molecules, increasing gut-blood and blood-brain barrier permeability. Cytokines mediate the activity of immune cells and may affect brain neurochemistry. The results of the present work serve as an additional support for the existence of an interrelationship between the nervous and immune system.