Beneficial effect of Toona sinensis Roemor on improving cognitive performance and brain degeneration in senescence-accelerated mice

Abstract

The purpose of the present study was to examine the effects of Toona sinensis Roemor extracts on antioxidative activities, brain morphological changes and cognitive ability. In an in vitro study, the antioxidant capacities of water extracts from Toona sinensis Roemor leaf (TSL), root (TSR) and bark (TSB) were evaluated by an a,a-diphenyl-b-pricryl-hydrazyl radical-scavenging test. The results showed that the scavenging activities of all Toona sinensis Roemor extracts were over 80 % at a concentration of 0·625 mg/ml. In an in vivo study, 3-month-old male senescence-accelerated-prone 8 mice were used as the tested subjects and fed four different diets: casein diet or casein diet supplemented with 1 % TSL, TSR or TSB extract for 12 weeks. The results showed that the mice supplemented with Toona sinensis Roemor extracts demonstrated significantly less amyloid b-protein deposition and lower levels of thiobarbituric acid-reactive substances than the control group. All Toona sinensis Roemor diet groups also showed better active shuttle avoidance responses, and higher superoxide dismutase, catalase and glutathione peroxidase activities, than the control group. It can thus be concluded that supplementation with either TSL, TSR or TSB extract could not only reduce the incidence of ß-amyloid plaques, but also improve learning and memory ability in senescence-accelerated-prone 8 mice. This might be due to the beneficial effects of Toona sinensis Roemor extracts on promoting the antioxidative defence system. Free radical-mediated reactions and reactive oxygen species have been proposed to be the major contributors to the pathological processes of neurodegenerative diseases such as Alzheimer's and Parkinson's disease. Alzheimer's disease is accompanied by cognitive impairment as well as involving the pathological build-up of extracellular, vascular and parenchymal deposits of a 40 -42-amino peptide, amyloid b-protein. It has been demonstrated that oxidative damage increased both in the brains of individuals with Alzheimer's disease (Friedlich & Butcher, 1994;Smith et al. 1997;Montine et al. 1999) and in b-amyloid plaque-forming transgenic mouse models of Alzheimer's disease Pappolla et al. 1998;Smith et al. 1998), suggesting that an elevated level of amyloid b-protein is sufficient to stimulate oxidative damage. In an in vitro study, a direct application amyloid b-protein to neuronal cells increased the production of H 2 O 2 (Behl et al. 1994), leading to amyloid b-protein neurotoxicity, which could be prevented by the use of antioxidants (Behl et al. 1992;Goodman et al. 1994).The development of rodent models of Alzheimer's disease will elucidate some important aspects of the aetiology of the disease and the development of therapeutic methods. In a murine model of accelerated senescence (senescence-accelerated mouse), severe senile amyloidosis is one of the most characteristic age-associated disorders (Higuchi et al. 2004). Ohta et al. (1989) and Flood & Morley (1993) have reported that the senescence-accelerated-prone 8 (SAM...

Anti-cancer and antioxidant properties of phenolics isolated from<i> Toona sinensis</i> A Juss acetone leaf extract

“…These data demonstrate that the phytochemicals in the extract were able to pass through the cell membrane. Liao et al [27] observed that the inhibitory 50 % concentration values in the DPPH radical-scavenging activity of TS leaf extracts was 0.209 mg/mL. Although the mechanism of different antioxidant activities vary, our results are nonetheless comparable to that of Liao et al [27].…”

The Senescence-accelerated Mouse (SAM): A Higher Oxidative Stress and Age-dependent Degenerative Diseases Model

“…Taken together, these innate subtle abnormalities in the mitochondrial respiratory chain might cause a gradual accumulation of oxidative damage in vital macromolecules in the cells, which eventually results in brain dysfunction at an older age. Successful interventions with melatonin [38], a-lipoic acid [39,40] and other antioxidants [41][42][43][44] further support the idea that oxidative stress and mitochondrial dysfunction are directly linked with the age-associated neurodegeneration phenotype of SAMP8 mice. A recent in vitro study suggests a mechanism for oxidative stress-induced neurodegeneration in SAMP8 brain [45].…”

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