Fig. 5

TGF-β1 mediates hOM-MSC to enhance neuroprotective function by activating the PI3K-Akt signaling pathway in microglia in vitro. a Western blotting measuring TGF-β1 protein expression in hOM-MSCs, and ALK protein expression in BV2 cells. b Exemplary immunofluorescence micrograph showing nuclei (DAPI), NeuN, and BAX expression in SH-SY5Y cells (Scale bars = 40 μm). c Western blotting measuring BAX protein expression in SH-SY5Y cells, and α-Syn, IL-1β, CD206, and LC3B protein expression in BV2 cells. d The histogram showing the BAX fluorescence expression in (b), and BAX, α-Syn, IL-1β, CD206, and LC3B protein expression in (c). e, f Western blotting measuring p-PI3K, p-Akt, p-mTOR, p50, p65, and LC3B protein expression in BV2 cells. Data are represented as mean ± SEM. ^*P < 0.05, ^**P < 0.01, ns non-significant. hOM-MSCs hypoxia-olfactory mucosa mesenchymal stem cells, TGF-β1 transforming growth factor-β1, ALK anaplastic lymphoma kinase, NeuN neuron-specific nuclear protein, DAPI 4’,6-diamidino-2-phenylindole, α-Syn α-synuclein, IL-1β interleukin-1β, PI3K phosphoinositide 3-kinase, Akt protein kinase B, mTOR mammalian target of rapamycin