Abstract
Movement disorders are the heterogeneous group of disorders characterized by the progressive and selective impairment in motor function. Movement disorders like Huntington's disease (HD) and Tardive dyskinesia (TD) share many common features at both cellular and subcellular levels. Filgrastim is a recombinant methionyl granulocyte colony-stimulating factor (GCSF), shows neuroprotective properties in in-vivo models of movement disorders. The present study was designed to evaluate the neuroprotective effect of filgrastimin the animal models of haloperidol and 3-NP induced neurotoxicity in rats. Study was divided in two different protocol, in study one, rats were administered with haloperidol for 21 days, and filgrastim at the dose of (20, 40 & 60 µg/kg,s.c.) was administered once a day, before haloperidol treatment and the following parameters (orofacial movements, rotarod, actophotometer) were assessed for TD. Similarly, in second study rats were administered with 3-NP for 21 days and filgrastimat the dose of (20 & 40 µg/kg, s.c.) was administered, and following parameters (rotarod, narrow beam walk and open field test) were assessed for HD. In each study, on 22nd day, animals were sacrificed, to isolate cortex and striatum for oxidative stress (LPO, GSH, SOD, catalase, and nitrate) parameters. The result revealed that haloperidol and 3-NP treatment significantly impaired motor coordination, oxidative defense and induce TD and HD like symptoms. Filgrastim pre-treatment significantly averted haloperidol & 3-NP induced behavioral and biochemical alterations, respectively. Conclusively, neuroprotective effect of filgrastim is credited to its antioxidant properties, hence filgrastim might be a novel therapeutic candidate to manage TD & HD.
Neuroprotective Effect of IND1316, an Indole-Based AMPK Activator, in Animal Models of Huntington Disease
