Abstract
This work aims to evaluate the antioxidant and protective effect of Raphia hookeri (Rh) fruit extracts and powders against aluminum induced neurotoxicity in rats. Extracts and powder were prepared using fruit mesocarp. Phytochemical contents (phenolic content and flavonoïd) and antioxidant in vitro activity were evaluated through the DPPH radical scavenging capacity, the ability to reduce ferric ion and Hydroxyl radical scavenging ability. The neurocognitive dysfunction, the activity of acetylcholinesterase (AChE) and activities of antioxidant in vivo indices were evaluated in the plasma, liver and brain of aluminum chloride (AlCl3) induced neurotoxicity in rats. The highest total phenolic (76.34 mg Eq AG/g of extract), flavonoïds’ contents (13.32 mg Eq CAT/g of extract), the best DPPH scavenging activity and the ability to reduce ferric ion (Fe3+) were obtained with aqueous extract. The administration of aqueous extract (200 and 400 g/kg bw) and powder (5% and 10 %) during 28 days resulted in a significant decrease (P Treatment with aqueous extract and powder of Rh mesocarp ameliorated neurobehavioral changes by enhancing antioxidant activities, cognitive functions. Therefore Rh would protect oxidative damage and preserve neurone functions.
Highlights
Aerobic cellular metabolism continuously produces reactive oxygen species (ROS) with concomitant potential for mutagenic and oncogenic effects
The evaluation of some biochemical parameters shows the decrease of malondialdehyde, nitric oxide and acetylcholine esterase activity and the increase of total protein level, catalase activities (CAT), superoxide dismutase (SOD) and glutathione level in plasma, liver and brain compared to the positive control group (PC)
The food staple was composed as follows: corn flour (77.8%), fish flour (20%), bone flour (0.1%), palm olein (1%), vitamins (0.1%), and salt (1%). 20 g of Raphia hookeri (Rh) powder was extracted into 200 ml of water and the mixture was regularly shaken during the extraction. 20 g of powder was extracted into 200 ml of ethanol, water and hydroethanolic (20/80) solvent respectively
Summary
Aerobic cellular metabolism continuously produces reactive oxygen species (ROS) with concomitant potential for mutagenic and oncogenic effects. The imbalance between ROS and antioxidants induces oxidative stress. This oxidative stress is implicated in several degenerative disorders such as: pathogenesis in inflammatory, partial ischemia, metabolic and denatured cranial nerve disease [1]. Brain tissues are highly susceptible to oxidative damage, probably because of its high oxygen consumption rate (20%), the presence of abundant polyunsaturated fatty acids in cell membranes, high iron (Fe) content, and low enzymatic antioxidants’ activities [3]. Aluminum is one of the well-known environmental heavy metal agents that affect the brain development, it can induce oxidative damage through multiple mechanisms such as binding to negative charged brain phospholipids, which contain polyunsaturated fatty acids and are attacked by reactive oxygen species (ROS) [4]. Aluminum has the potential to be neurotoxic in humans and animals, and is present in many manufactured foods and medicines [5]
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