Fig. 7

Pioglitazone treatment decreases the rate of neuroinflammation in the midbrain and striata of Cox10/DAT-cre mice. a-b double immunohistochemistry with antibody anti-TH and anti-Iba1 on midbrain slides of DAT-cre and Cox10/DAT-cre mice untreated a and treated with pioglitazone for 4 months b. Iba1+ cells are numerous in Cox10/DAT-cre midbrain sections and comparable to DAT-cre mice after pioglitazone treatment. Scale bar = 50 μm. c double immunohistochemistry with antibody anti-Iba1 and anti-CD11b (marker of activated microglia) on midbrain slides of 6 months old untreated Cox10/DAT-cre mice. Scale bar = 50 μm. d Immunohistochemistry with Ab anti-Iba1 on midbrain slides of Cox10/DAT-cre mice untreated and treated with pioglitazone. Red dashed line surrounds the substantia nigra. Black squares indicate the three regions chosen for Iba1+ cells counting. Enlargement of left black square shows numerous Iba1+ cells in Cox10/DAT-Cre mice. Scale bar = 50 μm. e Immunohistochemistry with Ab anti-GFAP on midbrain slides of Cox10/DAT-cre mice untreated and treated with pioglitazone. Enlargement shows no change of GFAP+ cells in Cox10/DAT-Cre mice. Scale bar = 50 μm. f: Microglial cells counting shows an increase of Iba1+ cells in Cox10/DAT-Cre midbrain at 2 and 6 months of age and a decrease after pioglitazone treatment (n = 3-6/group). g: Western blot and relative quantification of MHC-II, marker of activated microglia, in midbrain and striata of 2 and 4 months old DAT-cre and Cox10/DAT-cre mice (n = 3/group). h: Western blotting probing for markers of neuroinflammation (GFAP, Iba1, MHC-II) in striatal homogenates of DAT-cre and Cox10/DAT-cre mice untreated (untr) or treated with pioglitazone (PIO). Quantification of MHC-II normalized for GAPDH shows a decrease of glial activation after treatment with pioglitazone (n = 3/group)