Objective: In this study, we investigated the role of prostaglandin E2 inhibition, pro-inflammatory cytokine concentration and microglial activation in a Parkinsonian rat

Background: Neuro-inflammation plays a role in the microenvironment disturbance in Parkinson’s disease (PD). Cytokine and non-cytokine induced pathways affect glial cell activation following injury. Prostaglandin E2 has been implicated in the non-cytokine response to inflammation. This raises the question of whether manipulation of the inflammatory response pathways could lead to therapeutic interventions for PD

Methods: Male Sprague Dawley rats were lesioned stereotaxically with 6-OHDA. Bromelain which inhibits PGE2 was used to treat a subset of the rats, pre-lesion, 24 and 72hrs post- lesion. Behavioural assessments using the Open field, cylinder and step tests were carried out. Systemic and striatal concentration of pro-inflammatory cytokines and the quantification of cd11b/cd86 as a measure of glial cell activation were assessed

Results: 6-OHDA injection resulted in marked motor impairment which was alleviated by pre-lesion bromelain treatment. Bromelain treatment also resulted in the suppression of both systemic and striatal pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) as well as changes indicative of suppression of gliosis

Conclusions: Bromelain treatment reveals interconnectivity between the cytokine and non-cytokine mediated neuro-inflammatory pathways suggesting that PGE2 inhibition plays a role in protecting against dopamine neurodegeneration and may therefore be considered as part of a therapeutic strategy used to attenuate PD disease progression.

References: HIRSCH E.C AND HUNOT S. 2009. Neuroinflammation in Parkinson’s disease: A target for neuroprotection? Lancet Neurol. 8: 382–397.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/effects-of-pge-inhibition-on-striatal-neuroinflammation-in-6-ohda-lesion/