Abstract
Wild ginseng has better pharmacological effects than cultivated ginseng. However, its industrialization is limited by the inability to grow wild ginseng on a large scale. Herein, we demonstrate how to optimize ginseng production through cultivation, and how to enhance the concentrations of specific ginsenosides through fermentation. In the study, we also evaluated the ability of fermented cultured wild ginseng root extract (HLJG0701-β) to inhibit acetylcholinesterase (AChE), as well as its neuroprotective effects and antioxidant activity. In in vitro tests, HLJG0701-β inhibited AChE activity and exerted neuroprotective and antioxidant effects (showing increased catalyst activity but decreased reactive oxygen species concentration). In in vivo tests, after HLJG0701-β was orally administered at doses of 0, 125, 250, and 500 mg/kg in an animal model of memory impairment, behavioral evaluation (Morris water maze test and Y-maze task test) was performed. The levels of AChE, acetylcholine (ACh), blood catalase (CAT), and malondialdehyde (MDA) in brain tissues were measured. The results showed that HLJG0701-β produced the best results at a dose of 250 mg/kg or more. The neuroprotective mechanism of HLJG0701-β was determined to involve the inhibition of AChE activity and a decrease in oxidative stress. In summary, both in vitro and in vivo tests confirmed that HJG0701-β administration can lead to memory improvement.
Highlights
We evaluated the ability of a fermented cultured wild ginseng roots extract, HLJG0701-β, to inhibit AChE activity and assessed its neuroprotective and antioxidant effects using a scopolamine and ovariectomized (OVX) +
The total concentration of ginsenosides in cultured wild ginseng root treated with jasmonate was 188.06 ± 4.98 mg/g
The treatment (HLJG0701-β 125, 250 mg/kg) groups (0.906 ± 0.025, 0.942 ± 0.054 nmol) showed a clear reversal of the decrease in the OVX + D-galactose group (p < 0.05). These results indicate that administration of HLJG0701-β suppressed the increase in AChE activity and the reduction of ACh levels induced by OVX + D-galactose
Summary
Dementia is a symptom of neurodegenerative diseases including Alzheimer’s disease (AD) [1]. Typical symptoms of AD include memory loss, depression, lapses in judgment, confusion, and cognitive loss [2,3]. Metal ion homeostasis, mitochondrial dysfunction, neuroinflammation, apoptosis, endoplasmic reticulum dysfunction, and cell cycle imbalance have been implicated in the development of AD [2,4]. Aβ25-35 accumulates in cells due to the effects of reactive oxygen species (ROS), such as hydrogen peroxide (H2 O2 ) generated in vivo through metabolic processes, superoxide anions, hydroxyl radicals, etc., which can cause DNA damage, protein oxidation, and lipid peroxidation, resulting in cell dysfunction, the collapse of cell membrane fluidity, and apoptosis, leading to AD [7]
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