Fig. 6.

Post-ischemic NMN treatment prevents overexpression of NAD⁺ salvage pathway enzymes. Immunoreactivity of nicotinamide phosphoribosyl transferase (Nampt) and cytosolic Nicotinamide mononucleotide adenylyl transferase (Nmnat2) in mouse hippocampus. Animals were subjected to forebrain ischemia and treated with NMN (62.5 mg/kg) or vehicle (PBS) at the start of reperfusion. The rate-limiting enzyme of the NAD⁺ salvage pathway Nampt showed increased expression at early 2 h recovery period. The expression of the Nmnat2 enzyme showed tendency for increase, however the change was not significant when compared to sham animals. The ischemia-induced increase in expression was suppressed in NMN treated animals (A, B). Quantification of Nampt and Nmnat2 expression levels normalized to β actin (C, D). *p < 0.05, **p < 0.01 when compared to vehicle treated group, ##p < 0.01, ###p < 0.001 when compared to sham group (n = 8), ANOVA followed by Bonferroni’s test.