Fig. 6: Overexpression of miR-98 can reduce neuronal damages in ischemic stroke in in vtro and in vivo. | Cell Death & Disease

Fig. 6: Overexpression of miR-98 can reduce neuronal damages in ischemic stroke in in vtro and in vivo.

From: Neuronal extracellular vesicle derived miR-98 prevents salvageable neurons from microglial phagocytosis in acute ischemic stroke

Fig. 6

a The representative immunostaining of iNOS (green) and IBA1 (red) of mice brain slices 1d and 3d after ischemic stroke. The white arrows are iNOS and IBA1 colocalization. (scale bar = 200 μm). b–c The protein expression level of iNOS in microglia after OGD-R treatment and miR-98 agomir transfection, and quantification. d The lactate dehydrogenase (LDH) assay of microglia after OGD-R. e–f The protein expression level of PAFR in microglia after OGD-R treatment and miR-98 agomir transfection, and quantification. g The representative immunostainings (IBA1) of morphology of microglia. (Scale Bar = 50 μm). h–k The protein expression level of iNOS, PAFR and quantification. (n = 3 independent experiments). l–m The Nissl staining of cells of ipsilateral cortex and striatum and quantification. (n = 5 independent experiments). n–s The representative TTC stainings of the mice and rats brain sections and quantification of TTC stainings (N = 6 mice for each group, f rats for each group) and neurological function evaluations (N = 14 mice for each group, 20 rats for each group). t The schematic of neuronal EVs miR-98 transfer hypothesis between neurons and microglia after ischemic stroke. Data are shown as means±S.E.M., *P, #P < 0.05; **P, ##P < 0.01; ***P < 0.001 vs corresponding control.

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