BackgroundIn vitro antioxidant activities and neuron-like PC12 cell protective effects of solvent fractions from aged garlic extracts were investigated to evaluate their anti-amnesic functions. Ethyl acetate fractions of aged garlic had higher total phenolics than other fractions.MethodsAntioxidant activities of ethyl acetate fractions from aged garlic were examined using 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) diammonium salt (ABTS) and malondialdehyde (MDA) inhibitory effect using mouse whole brain homogenates. Levels of cellular oxidative stress as reactive oxygen species (ROS) accumulation were measured using 2',7'-dichlorofluorescein diacetate (DCF-DA). PC12 cell viability was investigated by 3-[4,5-dimethythiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) and lactate dehydtrogenase (LDH) assay. The learning and memory impairment in institute of cancer research (ICR) mice was induced by neurotoxic amyloid beta protein (Aβ) to investigate in vivo anti-amnesic effects of aged garlic extracts by using Y-maze and passive avoidance tests.ResultsWe discovered that ethyl acetate fractions showed the highest ABTS radical scavenging activity and MDA inhibitory effect. Intracellular ROS accumulation resulting from Aβ treatment in PC12 cells was significantly reduced when ethyl acetate fractions were presented in the medium compare to PC12 cells which was only treated with Aβ only. Ethyl acetate fractions from aged garlic extracts showed protection against Aβ-induced neurotoxicity. Pre-administration with aged garlic extracts attenuated Aβ-induced learning and memory deficits in both in vivo tests.ConclusionsOur findings suggest that aged garlic extracts with antioxidant activities may improve cognitive impairment against Aβ-induced neuronal deficit, and possess a wide range of beneficial activities for neurodegenerative disorders, notably Alzheimer's disease (AD).

The ethylacetate (EtOAc) fraction of blueberry leaf extract was investigated to examine the in vivo antiamnesic effects against amyloid β protein (Aβ)-induced learning and memory deficit. The fraction showed the highest antioxidant activities, and the generation of intracellular reactive oxygen species was significantly decreased. Cell viability assays revealed the in vitro cytoprotective effects of the fraction, and the cytoplasmic lactate dehydrogenase release into the medium was dose-dependently inhibited. In addition, a chlorogenic acid was identified as a predominant phenolic compound by high-performance liquid chromatography analysis. Antiamnesic effects were evaluated by using in vivo the Y-maze and passive avoidance tests, and preadministration of the fraction attenuated Aβ-induced memory impairment in both in vivo experiments. Acetylcholinesterase prepared from mice brain was inhibited by the fraction, and malondialdehyde generation in the brain homogenate was also decreased. These findings suggest that the EtOAc fraction of blueberry leaf extract could possess a wide range of physiological effects against neurodegenerative diseases.

To investigate neuronal cell protective effects of an ethyl acetate fraction from chestnut inner skin, in vitro assays, including 2 0 ,7 0 -dichlorofluorescein diacetate, 3-[4,5-dimethythiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT), and lactate dehydrogenase (LDH), were performed. Intracellular accumulation of reactive oxygen species resulting from hydrogen peroxide (H2O2) treatment of PC12 cells was significantly reduced when ethyl acetate fractions were present in the medium compared to PC12 cells treated with H2O2 only. In a cell viability assay using MTT, the ethyl acetate fraction protected against H2O2-induced neurotoxicity, and inhibited LDH release into the medium. In addition, the ethyl acetate fraction improved in vivo cognitive ability against amyloid b-peptide (Ab)-induced neuronal deficit. High-performance liquid chromatography analyses showed that gallic acid, catechin, and epicatechin were predominant phenolics in the ethyl acetate fraction. Consequently, the results suggest that chestnut inner skin, including above phenolics, could ameliorate Ab-induced learning and memory deficiency, and be utilized as effective substances for neurodegenerative disorders, notably Alzheimer's disease.

Extracts of rabbit-eye blueberries (Vaccinium virgatum) were investigated for in vitro neuroprotective and in vivo learning and memory effects in mice under trimethyltin (TMT)-induced neurotoxicity. Blueberry anthocyanins showed high in vitro antioxidant activities in ABTS and 2',7'-dichlorofluorescein diacetate (DCF-DA) assays. In a cell viability assay using MTT, anthocyanins showed protective effects, and lactate dehydrogenase release into the medium was effectively inhibited. Druginduced cognitive deficits, examined in vivo using Y-maze and passive avoidance testing, were ameliorated by the anthocyanin fraction. HPLC analysis showed that delphinidin was the predominant anthocyanin. After behavioral testing, acetylcholinesterase (AChE) activities and lipid peroxidation in the mouse brain were investigated for biochemical changes. Administration of blueberry anthocyanins reduced the level of TMT-induced memory injury via inhibition of the AChE activity and lipid peroxidation.

To find a neuroactive compound with a potent inhibitory effect on acetylcholinesterase (AChE) and in vivo anti-amnesic activity from natural resources, we evaluated anthocyanins and nonanthocyanins from black soybean extract. Nonanthocyanins from black soybean extract were the most potent and dose-dependent AChE inhibitors. Intracellular reactive oxygen species accumulation resulting from H2O2 treatment was significantly decreased compared with cells treated with H2O2 only. Nonanthocyanins were also neuroprotective against H2O2 treated neurotoxicity by 3-[4,5-dimethythiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assay. Finally, nonanthocyanins from black soybean in the preadministration group attenuated trimethyltin (TMT)-induced memory injury in both in vivo tests. AChE, prepared from mice brain tissues, was inhibited by nonanthocyanins from black soybean in a dose-dependent manner. Malondialdehyde generation in the brain homogenates of mice treated with nonanthocyanins from black soybean was decreased. We concluded that nonanthocyanins from black soybean had an efficacious in vitro AChE inhibitory activity, and protected against H2O2-induced neurotoxicity. In addition, our findings suggest that nonanthocyanins from black soybean may improve the TMT-induced learning and memory deficit because of AChE inhibition of mice brain tissue. Consequently, these results demonstrate that the nonanthocyanins from black soybean could possess a wide range of beneficial activities for neurodegenerative disorders.KEY WORDS: acetylcholinesterase black soybean cognitive function Glycine max (L.) Merr. syringic acid trimethyltin INTRODUCION Soybean (Glycine max) has been one of the long important nutritional sources since ancient times. Soybeans are extremely versatile and can be made into a variety of foods. Asians including Koreans consume an average of 20 to 80 g of traditional soy foods daily, the most common of which include tofu, miso, and tempeh. Americans consume much less soy, only about 1 to 3 g daily, and this is mostly in processed forms such as soy drinks, breakfast cereals, energy bars, and soy burgers.