Haifeng Zhai

Neurotrophic activity of honokiol on the cultures of fetal rat cortical neurons

Honokiol, a main biphenyl neolignan of the traditional crude medicine, Magnoliae cortex, was found to show neurotrophic activity on the cultures of rat cortical neurons at concentration from 0.1 to 10 microM. In the cortical neurons cultured in serum-free medium supplemented with B27, honokiol could promote neurite outgrowth. In addition, the survival and growth of neurons were significantly enhanced by adding honokiol to the primary cultures in serum-free medium supplemented with N2. Its neurotrophic activity was comparable to 40 ng mL(-1) of bFGF at concentration of 10 microM.

Honokiol and magnolol induce Ca2+ mobilization in rat cortical neurons and human neuroblastoma SH-SY5Y cells

We examined the intracellular Ca(2+) response in primary cultured rat cortical neurons and human neuroblastoma SH-SY5Y cells by Fluo 3 fluorescence imaging analysis. In these two kinds of neuronal cells, honokiol and magnolol increased cytoplasmic free Ca(2+) with a characteristic lag phase. The cytoplasmic free Ca(2+) increase was independent of extracellular Ca(2+), but dependent on activation of phospholipase C and inositol 1,4,5-triphosphate (IP(3)) receptors. These results suggest that honokiol and magnolol increase cytoplasmic free Ca(2+) through a phospholipase C-mediated pathway, and that the release of Ca(2+) from intracellular stores mainly contributes to the increase in cytoplasmic free Ca(2+). Thus, honokiol and magnolol may be involved in a new activation mechanism closely associated with intracellular Ca(2+) mobilization.

Neuroprotective effect of magnolol in the hippocampus of senescence-accelerated mice (SAMP1)

Abstract We investigated age-dependent neuronal loss in the hippocampus and the protective effect of magnolol using SAMP1 mice in comparison with SAMR1. SAMP1 and SAMR1, 2 to 10 months old, were used. Magnolol (2 and 5 mg/kg) was orally administered once a day for 7 days to 2-month-old mice and evaluation was carried out at 4 months. The density of neurofibrils and axons decreased with aging in the CA1 and CA3 regions of the hippocampus. The rate of decrease in SAMP1 was greater than that of SAMR1. Treatment with magnolol dose-dependently prevented the decrease of density in CA1 and CA3 at 4 months. However, until the age of 4 months, SAMP1 animals did not behaviorally differ from SAMR1 either with or without magnolol. It has been suggested that imbalance between the rates of generation and utilization of reactive oxygen species (ROS) and organic free radicals may be one of the main reasons for accelerated aging of SAMP1 animals. These findings suggest that the antioxidant and free radical scavenging activity of magnolol may contribute to the protective effect against neuronal loss in the hippocampus.