Abstract

BackgroundOxidative stress is known to contribute to the mechanisms underpinning the pathogenesis of neurodegenerative diseases. Previous studies have identified the presence of flavonoids as the major constituents of Passiflora edulis (PE) with antioxidant activity. This work aims at investigating the antioxidant, anti-neuroinflammatory, and neuroprotective effect of three PE fruit extracts, flavonoid fraction, and juice on neurodegenerative rat model.MethodsExtracts were prepared using fruit pulp and peel and juice using pulp. Phytochemical contents (phenolic content and flavonoid) and in vitro antioxidant activity were evaluated through the DPPH radical scavenging capacity and the ability to reduce ferric ion. The neurocognitive dysfunction, activity of acetylcholinesterase (AChE), levels and activities of in vivo oxidant–antioxidant indices as well as neuroinflammatory markers were evaluated in the hippocampus and cortex of aluminum chloride (AlCl3) induced Alzheimer’s rats (AD).ResultsThe highest total phenolic and flavonoids’ contents, the best DPPH scavenging activity and the ability to reduce ferric ion (Fe3+) were obtained with peel aqueous extract. The administration of the peel aqueous extract, juice, and flavonoid fraction resulted in a significant decrease (P < 0.05) in plasma and tissue levels of malondialdehyde compared to the positive control (PC). The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), cycyclooxygenase-2 (COX-2), and amyloid ß-42 (ß-42) were significantly reduced whereas the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione level were significantly higher in the treated than that in the untreated Alzheimer’s rats (PC) groups (P < 0.05), respectively, in the hippocampus and in plasma, brain, and liver homogenates following the administration of juice, flavonoid fraction, and extracts (both doses). Treatment of AD-rats with PE ameliorated neurobehavioral changes, as evidenced by the improvement in brain function, as well as, modulation of AChE, and confirmed by the histological changes and Morris water maze test. The effect of aqueous extract was slightly greater than that of the flavonoids fraction, thus suggesting that flavonoids account for most of the Passiflora edulis antioxidant activity and neuroprotective effect.

Highlights

  • Oxidative stress is known to contribute to the mechanisms underpinning the pathogenesis of neurodegenerative diseases

  • Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disease characterized by the presence of intracellular amyloid aggregates and extracellular neurofibrillary tangles which results in neurocognitive decline and memory impairment

  • HP presented the greatest value of phenolic compounds and flavonoids (54.6 ± 3.84 mg GAE/g of extract and 29.78 ± 3.1 mg CE/g of extract respectively), followed by HEG (38.25 ± 1.98 GAE mg/g of extract) and the EP (33.8 ± 0.82 mg GAE/g of extract)

Read more

Summary

Introduction

Oxidative stress is known to contribute to the mechanisms underpinning the pathogenesis of neurodegenerative diseases. Previous studies have identified the presence of flavonoids as the major constituents of Passiflora edulis (PE) with antioxidant activity. Oxidative stress is the primary cause of pathogenesis in inflammatory, partial ischemia, metabolic, and denatured cranial nerve disease [1]. Brain tissues are highly susceptible to oxidative damage, probably because of high oxygen consumption rate (20%), the presence of abundant polyunsaturated fatty acids in cell membranes, high iron (Fe) content, and low enzymatic antioxidants’ activities [2]. Aluminum is one of the well-known environmental heavy metal agents that affect the brain development. It is a relatively low redox mineral, it can induce oxidative damage through multiple mechanisms. Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disease characterized by the presence of intracellular amyloid aggregates and extracellular neurofibrillary tangles which results in neurocognitive decline and memory impairment

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call