Imidazolium Salt (DBZIM) Reduces Gliosis in Mice Treated with Neurotoxicant 2′-CH3-MPTP

Abstract

We have recently identified a class of imidazolium salts (IMSs) with antioxidative property and can function as scavengers for radical oxygen species (ROS) [18]. Here, we investigate one of the IMSs, 1,3-bisbenzylimidazolium bromide (DBZIM), for its possible role in attenuating neurotoxicity and gliosis in the retina and the brain induced by a Parkinsonian neurtoxicant, methyl-4(2'-methylphenyl)-1,2,3,6-tetrahydropyridine (2'-CH(3) -MPTP), which is a free radical generating agent. In this study, we employ a molecular retinal imaging method, which we recently developed in a transgenic mouse model expressing green fluorescent protein (GFP) under the control of glial fibrillary acidic protein (GFAP) promoter [14], to assess the efficacy of DBZIM, since currently no in vitro system with a sufficient complexity is available for accurately assessing a compound's efficacy. The longitudinal imaging results showed DBZIM can effectively suppress the neurotoxicant-induced retinal gliosis. Immunohistochemistry performed on the postmodern mouse brain confirmed that DBZIM also reduced striatal gliosis, and concomitantly attenuated the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). These findings suggest that DBZIM could be a useful small molecular compound for studying neurotoxicity and neuroprotection in the retina and the brain.

Imidazolium salts and their polymeric materials for biological applications

“…With its promising antioxidative property, 16 was also demonstrated to have a possible role in attenuating neurotoxicity and gliosis in the retina and the brain, as induced by a Parkinsonian neurotoxicant, methyl-4(2 0 -methylphenyl)-1,2,3,6tetrahydropyridine (2 0 -CH 3 -MPTP), a free radical generating agent. 57 In this study, the authors employed a molecular retinal imaging method to assess the efficacy of 16. The longitudinal imaging results showed that 16 can effectively suppress the neurotoxicant-induced retinal gliosis.…”

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