Biol. Pharm. Bull., 28(9),1762-1765, September 2005

Notes

Neurotrophic Effect of Magnolol in the Hippocampal CA1 Region of Senescence-Accelerated Mice (SAMP1)

Nobuaki MATSUI,^*,a Hiroshi NAKASHIMA,^a Yuki USHIO,^a Toshimasa TADA,^a Akiko SHIRONO,^a Yoshiyasu FUKUYAMA,^a Kousuke NAKADE,^a Haifeng ZHAI,^a Yumiko YASUI,^a Nobuyuki FUKUISHI,^a Reiko AKAGI,^b and Masaaki AKAGI^a

^a Faculty of Pharmaceutical Sciences, Tokushima Bunri University; Yamashiro-cho, Tokushima 770-8514, Japan: and ^b Faculty of Health and Welfare Science, Okayama Prefectural University; Kuboki, Souzya 719-1197, Japan. * To whom correspondence should be addressed. e-mail: matsui@ph.bunri-u.ac.jp

Magnolol has neurotrophic effects in primary cultured rat cortical neurons, which are expressed as the promotion of neurite outgrowth and neuronal survival. In this study, we investigated the protective effect of magnolol against age-related neuronal loss in the hippocampus using senescence-accelerated mouse (SAMP1). Magnolol (5, 10 mg/kg) was orally administered once a day for 14 d to 2- or 4-month-old mice, and evaluation was carried out when the mice were 4 or 6 months old. The density of neurofibrils decreased with aging in the stratum radiatum of the CA1 region in the hippocampus of SAMP1, not SAMR1. Treatment with magnolol significantly prevented the decrease of neurofibrils in the CA1, when it was administered in 2-month-olds. However, administration at 4 months of age did not result in a preventive effect. These findings suggest that the administration of magnolol before the initiation of neuronal loss may result in a protective effect in the hippocampus.

Key words magnolol; hippocampus; senescence accelerated mouse