The DAAO was specifically expressed in astrocytes, and its double immunostaining with the astrocytic intracellular marker, glial fibrillary acidic protein, in the cortical peri-infarct area was up-regulated following ischaemic insult, with peak increase on Day 5 after MCAO.
Here we showed that phosphorylated signal transducer and activator of transcription 3 (STAT3) level increased along with that of the astrogliosis marker glial fibrillary acidic protein (GFAP) on days 1, 3, and 14 post-reperfusion in 9-month-old male mice with middle cerebral artery occlusion (MCAO).
In addition, after treatment, the MCAO rats showed decreased NSS and mRNA and protein expression of nestin, but elevated mRNA and protein expression of NeuN, β‑III‑Tub and GFAP at the 2nd, 4 and 8th weeks, and decreased positive expression of HNA and nestin with enhanced expression of NeuN, β‑III‑Tub and GFAP.
Activation of striatal microglia and astrocytes was observed with immunohistochemistry of ionized calcium binding adaptor molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP) at 2, 3, and 7 days after MCAO.
Methyllycaconitine treatment increased cytomembrane FGFR1 expression and GFAP/BrdU-positive cells, upregulated the levels of phosphoinositide 3-kinase (PI3K) and phospho-Akt (pAkt), decreased nuclear FGFR1 expression, decreased the number of DCX-positive cells, and reduced the levels of DCX, PSA-NCAM, and Mash1 in the SVZ of MCAO mice compared with levels in vehicle-treated MCAO mice.
The pretreatment of TA showed a marked reduction in infarct size, improved neurological function, suppressed neuronal loss, and downregulated the GFAP expression in MCAO rats.
The densities of GFP+/ glial fibrillary acidic protein (GFAP)+ astrocytes and GFP+/O4+ oligodendrocytes were reduced in the striatum following MCAO (4.8 +/- 1.02 vs. 2.5 +/- 0.4 cells/high-power field, HPF; p = 0.005; 2.8+/- 1 vs. 0.5 +/- 0.2 cells/HPF, p = 0.008).