This study was designed to compare the chemical compositions and effect of essential oils from the peels and seeds of sweet orange on cholinergic (acetylcholinesterase [AChE], butyrylcholinesterase [BChE]) and monoaminergic (monoamine oxidase [MAO]) enzymes. The ability of the essential oils to protect the brain against Fe2+‐induced lipid peroxidation was also investigated. Forty and forty‐four compounds were identified in peels and seed essential oils, respectively, using gas chromatography. The essential oils inhibited AChE, BChE and MAO in dose‐dependent manner. However, essential oil from the peels had higher inhibition on cholinergic enzymes but lower inhibitory effect on MAO and Fe2+‐induced lipid peroxidation compared to the seed essential oils. This study also revealed the presence of volatile compounds. Conclusively, both essential oils could be used as therapeutic agents in the management of Alzheimer's disease.
Practical Applications
Sweet orange (Citrus sinensis) peels and seeds are waste materials in the production of orange juice and can be used as a source to produce essential oils which can be of use in the production of functional foods and nutraceuticals. This study provided reference information for the first time on the chemical composition and potential application of sweet orange peels and seed essential oils in the treatment and management of Alzheimer's diseases.
Green leafy vegetable is one of the major cuisines in Southern Nigeria and they are not only consumed for their palatability, but also for their nutritional and medicinal properties as reported in folklore. Notable among them are afang (Gnetum africanum), editan (Lasianthera africana) and utazi (Gongronema latifolium). In this study, we investigated the effect of aqueous extracts from afang, editan and utazi leaves on cholinesterases [acetylcho linesterase (AChE) and butyrylcholinesterase (BChE)] and monoamine oxidase (MAO) activities. Fe 2+ chelating abilities were also determined as an assessment of their neuroprotective potentials in vitro. We also assayed for their total phenol contents while the constituent phenolics were characterized using high performance liquid chromatography coupled with diode array detector (HPLC-DAD). The results revealed that the extracts inhibited AChE, BChE and MAO activities and also chelated Fe 2+ in concentration dependent manner. The HPLC-DAD char acterization showed that gallic, caffeic and ellagic acids and rutin were the dominant phenolic compounds in the extracts; nevertheless, utazi had the highest distribution of identified phenolics while afang had the least. The ability of the aqueous extracts of the vegetables to inhibit key enzymes (AChE, BChE and MAO) relevant to neu rodegeneration, as well chelate metal ion could help suggest their possible neuroprotective properties. These vegetables could be use as dietary intervention in the management of neurodegenerative diseases such as Alzheimer's and Parkinson's diseases.
Background. This study sought to investigate the antidiabetic and antihypertensive mechanisms of cocoa (Theobroma cacao) bean through inhibition of α-amylase, α-glucosidase, angiotensin-1 converting enzyme, and oxidative stress. Methodology. The total phenol and flavonoid contents of the water extractable phytochemicals from the powdered cocoa bean were determined and the effects of the extract on α-amylase, α-glucosidase, and angiotensin-1 converting enzyme activities were investigated in vitro. Furthermore, the radicals [1,1-diphenyl-2 picrylhydrazyl (DPPH), 2,2..-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid) (ABTS), hydroxyl (OH), and nitric oxide (NO)] scavenging ability and ferric reducing antioxidant property of the extract were assessed. Results. The results revealed that the extract inhibited α-amylase (1.81 ± 0.22 mg/mL), α-glucosidase (1.84 ± 0.17 mg/mL), and angiotensin-1 converting enzyme (0.674 ± 0.06 mg/mL [lungs], 1.006 ± 0.08 mg/mL [heart]) activities in a dose-dependent manner and also showed dose-dependent radicals [DPPH (16.94 ± 1.34 mg/mL), NO (6.98 ± 0.886 mg/mL), OH (3.72 ± 0.26 mg/mL), and ABTS (15.7 ± 1.06 mmol/TEAC·g] scavenging ability. Conclusion. The inhibition of α-amylase, α-glucosidase, and angiotensin-1 converting enzyme activities by the cocoa bean extract could be part of the possible mechanism by which the extract could manage and/or prevent type-2 diabetes and hypertension.
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