FIGURE 6.

hPMSCs‐derived ACE‐2 products maintain blood perfusion in MCAO mice independent of AT2 receptors. A, Laser speckle measurement of brain perfusion showed no significant differences in total perfusion between PD‐pretreated MCAO (n = 5) and MCAO (n = 6) mice (not significant [NS], P > .99). Significant increases in blood flow into the brain of PD‐pretreated MCAO+hPMSCs (n = 5) mice were observed compared to PD‐pretreated MCAO (**P = .001). B, Significant elevation of blood perfusion observed in the ipsilateral hemisphere of PD‐MCAO+hPMSC mice compared to PD‐MCAO group (**P = .001). C, Significant increase of blood flow into the contralateral hemisphere of hPMSC‐treated PD‐MCAO (*P = .01) observed in comparison with untreated PD‐MCAO mice. There were no significant changes in (B) ipsilateral (NS, P > .99) and (C) contralateral (NS, P = .79) perfusion of MCAO vs PD‐MCAO mice. Two‐tailed Student's t test analysis did not show any significant differences in blood flow between the ipsilateral (NS, P = .55; C) and contralateral (NS, P = .55; D) hemispheres of PD‐pretreated MCAO, regardless of hPMSCs treatment. D, Two‐way analysis of variance (ANOVA) revealed significant disturbances in blood perfusion between ipsilateral and contralateral hemispheres of MCAO (*P = .01) and PD‐MCAO (*P = .03) groups. No significant differences were detected between ipsilateral and contralateral perfusion of sham (NS, P > .99), MCAO+hPMSC (NS, P = .75), and PD‐MCAO+hPMSC (NS, P = .58). All graph data show the means ± SEM. ACE‐2, angiotensin converting enzyme‐2; hPMSCs, human placenta mesenchymal stem cells; MCAO, middle cerebral artery occlusion