Figure 4

From: Candesartan, an Angiotensin II AT1-Receptor Blocker and PPAR-γ Agonist, Reduces Lesion Volume and Improves Motor and Memory Function After Traumatic Brain Injury in Mice

Figure 4

Candesartan treatment modulates TGFβ1 and TGFβ3 expression after CCI. TGFβ1 immunoreactivity (red) was decreased by candesartan treatment in the ipsilateral cortex (b) and hippocampus (d) in comparison with that in vehicle-treated mice (a, c, respectively). (f) Quantitative analysis of TGFβ1 immunoreactivity showed that candesartan treatment led to a reduction of TGFβ1 immunoreactivity of 47% in the cortex and 49% in the hippocampus compared with vehicle-treated groups (mean±SEM, n=4, *p<0.05). Conversely, candesartan treatment increased TGFβ3 immunoreactivity in the cortex (h) and hippocampus (j) in comparison with immunoreactivity in vehicle mice (g, i, respectively). (l) Quantitative analysis of TGFβ3 immunoreactivity showed that candesartan treatment led to an increase in TGFβ3 immunoreactivity of 50% in the cortex and 36% in the hippocampus compared with vehicle-treated groups (mean±SEM, n=4, *p<0.05). Higher magnification images show TGFβ1 and TGFβ3 colocalization with the astroglial marker, GFAP (e, k, respectively). Scale bars represent 50 μm (a–d and g–j) and 25 μm (e, k).