Testosterone Deficiency Accelerates Neuronal and Vascular Aging of SAMP8 Mice: Protective Role of eNOS and SIRT1
Figure 2
Supplementation of testosterone improves cognitive function in SAMP8 mice.
A. Escape latency and plasma testosterone level of male SAMR1 (N = 10) and SAMP8 mice (N = 10) at 18 months of age. These mice were implanted subcutaneously with a placebo or a 21-day-release 2.5 mg testosterone pellet in the dorsal neck. B. Number of SA-βgal-stained Leydig cells in testes in SAMR1 and SAMP8. Arrows indicate Leydig cells. Representative SA-βgal-stained testes from SAMR1 and SAMP8. C. Escape latency of castrated SAMR1 (upper, N = 5) and recipient SAMP8 (lower, N = 5). Observation (0–10 weeks) was started from 3 weeks after operation. D. SIRT1 expression in hippocampus of SAMP8 with or without DHT treatment. Immunofluorescent staining for SIRT1 (green) and DAPI (blue). E. Expression of AR in SAMR1 and SAMP8 brains. (*p<0.05).