Multiple compounds improve aged MDSPC proliferation (self-renewal).

<p>(A) Aged MDSPCs were cultured in medium containing aspirin, nordihydroguaiaretic acid (NDGA), or rapamycin, and proliferation was monitored by live cell imaging for up to 60 hours, or (B) cells were treated in fusion medium and assessed for myogenic differentiation after 5 days (*p≤0.05 Aged WT vs Treated; ANOVA followed by Tukey post-hoc analysis).</p

NF-κB inhibition decreases senescence in BM-MSCs.

<p>BM-MSCs were treated for 48 hours with IKK inhibitor VII and then stained for senescence-associated beta-galactosidase (SA β-gal) expression, which demonstrated a decrease in cell senescence (*p≤0.05, T-test).</p

NF-κB inhibition improves the differentiation of MDSPCs isolated from old mice.

<p>(A) Brightfield images demonstrate a dose dependent increase in myotube formation following IKKi administration (10x images). (B) Immunofluorescent staining for MyHC demonstrated significantly improved differentiation following treatment at the 5μM dose (20x magnification), quantified in (C). (D) The total number of nuclei per field of view for experiment in B, C (*p≤0.05; ANOVA followed by Tukey post-hoc analysis). (E) IKKi treatment of young WT MDSPCs did not significantly improve differentiation (*p≤0.05, T-test).</p

NF-κB inhibition improves the oxidative stress resistance of MDSPCs isolated from old mice.

<p>MDSPCs were exposed to 250 μM H₂O₂ and monitored by live cell imaging for up to 24 hours. IKKi treated aged WT MDSPCs and aged <i>p65</i>^+/- MDSPCs demonstrated improved survival compared to vehicle treated aged WT MDSPCs (*p≤0.05 Aged WT vs +IKKi; +p≤0.05 Aged WT vs Aged <i>p65</i>^+/-; ANOVA followed by Tukey post-hoc analysis).</p