Abstract
Background: Recent evidence indicates the critical role of neuroinflammation in the pathogenesis of SAH. Mesenchymal stem cells represent a new frontier in the treatment of numerous diseases and have been shown to have therapeutic effects in neurological disease model such as ischemic stroke. Methods: We employed a murine model of endovascular filament perforation for experimental SAH and tail vein injections were performed for hypoxic hUC-MSC secretome treatment and phosphate buffer treatment (control). The data were expressed as mean+/-SEM and statistical analyses were performed with IBM SPSS 23.0 software. Results: Microglia exhibited suppressed M1 polarization in hypoxic-hUC-MSC-secretome-treated mice at day 3 as compared to phosphate-buffer-treated mice. mRNA expressions of M1-polarization markers (CD16: 0.59+/-0.07; CD32: 0.62+/-0.11, p=0.024; CD68: 0.72+/-0.07. p=0.049) were downregulated and M2-polarization marker TREM2 expression were upregulated (1.57+/-0.13, p=0.013). Confocal microscopy at day 1 showed decreased CD16/32 expression in hypoxic-hUC-MSC-secretome-treated mice as compared to phosphate-buffer-treated mice, and CD206 positive cells were observed in hypoxic-hUC-MSC-secretome-treated mice. mRNA expression of IL-4 was upregulated in hypoxic-hUC-MSC-secretome-treated mice at day 1 as compared to phosphate-buffer-treated mice. Conclusions: Hypoxic hUC-MSC treatment had a positive effect in the modulation of neuroinflammation in a murine experimental SAH model and should be further investigated.
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