Fig. 6

TGF-β1 mediates hOM-MSC to facilitate the recovery of nerve function by activating the PI3K-Akt signaling pathway in microglia in vivo. a The neurologic function score of open field test showing the activity trace of PD mice (left). The slide scanning technique shows TH⁺ cells immunohistochemical micrograph (medium) and shows Iba1⁺ cells immunohistochemical micrograph in the SN of PD mice (right) (scale bars = 200 μm). b The neurologic function score of the open field test shows the histogram of total distance, average speed, and central time (n = 6), and the Tatarod test shows the histogram of total distance and escape latency (n = 6). c The histogram showing TH⁺ cell expression and the number of Iba1⁺ cells in (a). d Exemplary immunofluorescence micrograph showing nuclei (DAPI), AAV ALK-GFP, and Iba1 co-localization expression in microglia of SN in PD mice (scale bars = 20 μm). e, f Western blotting measuring p-PI3K, p-Akt, p-mTOR, p50, and p65 protein expression in SN of PD mice. Data are represented as mean ± SEM. ^*P < 0.05, ^**P < 0.01. TH tyrosine hydroxylase, GFP green fluorescent protein, PI3K Phosphoinositide 3-kinase, Akt protein kinase B, mTOR mammalian target of rapamycin, hOM-MSCs hypoxia-olfactory mucosa mesenchymal stem cells, PD Parkinson’s disease, TGF-β1 transforming growth factor-β1, ALK anaplastic lymphoma kinase, AAV adeno-associated virus