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Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Prostaglandin D2/J2 signaling pathway in a rat model of neuroinflammation displaying progressive parkinsonian-like pathology: potential novel therapeutic targets

Fig. 8

Ibuprofen (IBP) ameliorates the PD-like pathology induced by PGJ2 except for astrocyte activation. a Ibuprofen treatment starting the day after the first surgery reduces TH+ (blue, dopaminergic) neuronal loss and Iba1+ (red, microglia) activation, but not GFAP+ (green, astrocyte) reactivity in the SNpc at 4 weeks (4w) post two (2X) PGJ2-injections. Scale bar = 500 μm. b There was no statistical difference in TH+ DA neurons between ibuprofen-fed PGJ2-treated rats and ibuprofen-fed controls (DMSO-treated). The extent of PGJ2 damage was assessed by calculating the total number of TH + neurons (mean ± SEM) in the SNpc using unbiased stereology as described in Materials and Methods. c, d There was no statistical difference between the number of reactive (c) or amoeboid (d) microglia in ibuprofen-fed PGJ2-treated rats and ibuprofen-fed controls (DMSO-treated). e Astrocyte reactivity is significantly higher in ibuprofen-fed PGJ2-treated rats than in ibuprofen-fed controls (DMSO-treated). For A through E, N = 3 rats per group. Values on the y-axis represent the ratios between the ipsilateral SNpc over the contralateral (in c and d normalized to the number of ramified microglia). f There was no statistical difference in motor asymmetry between ibuprofen-fed PGJ2-treated rats and ibuprofen-fed controls (DMSO-treated). For f, N = 6 to 9 rats per group. Black and gray circles, control, DMSO-treated rats; red and pink circles, PGJ2-treated rats. Statistical significance was estimated with Student’s T test to compare DMSO and PGJ2-treated groups. The p values in red indicate significant (p < 0.05) difference from DMSO-injected rats

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