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. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: Mol Neurobiol. 2015 Aug 2;53(7):4387–4396. doi: 10.1007/s12035-015-9347-3

Figure 4.

Figure 4

BMMNC transplantation reverses atherosclerosis-induced changes in antioxidant enzymes, eNOS, inflammatory response, and cell apoptosis. (A) Western blot analysis of eNOS in plaques. (B) Quantification analysis showed that plaques from the BMMNC group contained more eNOS than did plaques from the vehicle group. (C–F) BMMNC transplantation upregulated expression of the antioxidant enzymes GPx-1 and SOD-1 in plaque. (C, E) Western blot analysis of GPx-1 and SOD-1 in plaque. (D, F) Quantification of band densities showed that plaques from rabbits treated with BMMNCs had significantly higher GPx-1 and SOD-1 protein expression than did plaques from vehicle-treated rabbits. (G–H) BMMNC transplantation reduced expression of cell-death marker cleaved caspase-3 in plaque. (G) Western blot analysis of cleaved caspase-3. (H) Quantification analysis showed that cleaved caspase-3 was significantly lower in plaques from BMMNC-treated rabbits than in plaques from vehicle-treated rabbits. *p<0.05 vs. vehicle group. (I–L) BMMNC transplantation significantly decreased the mRNA expression of proinflammatory cytokines in plaque. (I) Representative RT-PCR bands showing mRNA expression of IL-1 β, TNF-α, and MMP-9 in plaque. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as a loading control. (J–L) Analysis of band optical densities showed that BMMNC transplantation significantly decreased the mRNA expression of IL-1 β, TNF-α, and MMP-9 compared with that in vehicle-treated animals. *p<0.05 vs. vehicle group. n=6 rabbits per group.