Abstract

BackgroundAlbizia adianthifolia (Schumach.) W. Wright (Fabaceae) is a traditional herb largely used in the African traditional medicine as analgesic, purgative, anti-inflammatory, antioxidant, antimicrobial and memory-enhancer drug. This study was undertaken in order to evaluate the possible cognitive-enhancing and antioxidative effects of the aqueous extract of A. adianthifolia leaves in the 6-hydroxydopamine-lesion rodent model of Parkinson’s disease.MethodsThe effect of the aqueous extract of A. adianthifolia leaves (150 and 300 mg/kg, orally, daily, for 21 days) on spatial memory performance was assessed using Y-maze and radial arm-maze tasks, as animal models of spatial memory. Pergolide - induced rotational behavior test was employed to validate unilateral damage to dopamine nigrostriatal neurons. Also, in vitro antioxidant activity was assessed through the estimation of total flavonoid and total phenolic contents along with determination of free radical scavenging activity. Statistical analyses were performed using two-way analysis of variance (ANOVA). Significant differences were determined by Tukey’s post hoc test. F values for which p < 0.05 were regarded as statistically significant. Pearson’s correlation coefficient and regression analysis were used in order to evaluate the association between behavioral parameters and net rotations in rotational behavior test.ResultsThe 6-OHDA-treated rats exhibited the following: decrease of spontaneous alternations percentage within Y-maze task and increase of working memory errors and reference memory errors within radial arm maze task. Administration of the aqueous extract of A. adianthifolia leaves significantly improved these parameters, suggesting positive effects on spatial memory formation. Also, the aqueous extract of A. adianthifolia leaves showed potent in vitro antioxidant activity. Furthermore, in vivo evaluation, the aqueous extract of A. adianthifolia leaves attenuated the contralateral rotational asymmetry observed by pergolide challenge in 6-OHDA-treated rats.ConclusionsTaken together, our results suggest that the aqueous extract of A. adianthifolia leaves possesses antioxidant potential and might provide an opportunity for management neurological abnormalities in Parkinson’s disease conditions.

Highlights

  • In the majority of SN-lesioned rats the point of the syringe needle was positioned in the central part of the SN and the lesions extended to a part of adjacent structures including substantia nigra pars reticulata, without any significant damage

  • The results strongly suggest that phenolics and flavonoids are important components of the A. adianthifolia leaves and this could explain their high radical scavenging activity (Table 1)

  • In the rotational behavioral test, analysis of variance (ANOVA) revealed an attenuation of asymmetric motor behavior (F(3,36) = 20.03, p < 0.0001) in experimental animals treated with the aqueous extract of A. adianthifolia leaves (150 and 300 mg/kg) in a dose-dependent manner as compared to control group (Figure 2)

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Summary

Introduction

This study was undertaken in order to evaluate the possible cognitive-enhancing and antioxidative effects of the aqueous extract of A. adianthifolia leaves in the 6-hydroxydopamine-lesion rodent model of Parkinson’s disease. Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease (AD), is characterized by motor and behavioral disturbances that include a resting tremor, postural instability and bradykinesia [1]. PD is often complicated by a variety of cognitive symptoms that range from isolated memory and thinking problems to severe dementia. While the motor symptoms of PD are well-known (tremor, rigidity, slowness of movement, imbalance), the commonly seen deficits in memory, attention, problem-solving, and language are less understood. Studies have shown that over 50% of people with PD experience some form of cognitive impairment. Memory problems in PD are typically milder than in Alzheimer’s disease. Non-motor symptoms in advanced stages of PD such as depression, dementia, sleep abnormalities and autonomic failure are probably the consequence of degeneration of both dopaminergic and non-dopaminergic systems, which still lacks efficacious treatments at present [4]

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