Ginseng berry exhibits a diverse range of pharmacological activities. The present study aimed to examine the neuroprotective effects of ginseng berry aqueous extract (GBE) against oxidative stress and to assess the impact of GBE on memory impairment in mice. In HT-22 cells, GBE pretreatment significantly inhibited glutamate-and hydrogen peroxide-mediated cytotoxicity in a concentration-dependent manner, while treatment with up to 100 µg/ml GBE alone did not change cell viability. In a murine model of scopolamine (SCP)-induced memory impairment, results from the passive avoidance test and the Morris water maze test indicated that GBE administration for 4 weeks prolonged step-through latency time and shortened escape latency time, suggesting that GBE can attenuate deficits in long-term memory induced by SCP. Additionally, GBE prevented SCP-induced reductions in acetylcholine by decreasing acetylcholinesterase activity and upregulating choline acetyltransferase mRNA levels in the hippocampus. GBE mitigated SCP-mediated mRNA decreases in brain-derived neurotrophic factor levels and its associated signaling molecules. Furthermore, GBE administration significantly suppressed malondialdehyde production and increased glutathione levels, catalase activity and superoxide dismutase activity in SCP-induced memory impaired mice. Therefore, the results of the current study indicated that ginseng berry may be a potential candidate for treating or preventing memory deficits that are associated with neurodegenerative disorders.
Vitamins are essential to human body, and 13 vitamins have been identified and classified as fat-soluble vitamins (A, E, D, and K) and water-soluble vitamins (B-group vitamins and vitamin C) according to their solubility (Turner & Mathiasson, 2000). In particular, fat-soluble vitamins are necessary for regulating various cell metabolisms, which include anti-oxidation, cell signaling, and the modulation of the immune system (Chadare et al., 2019; Turner, King, & Mathiasson, 2001). Vitamin A and its precursor, which is β-carotene, are predominantly found in plants, and they are mainly necessary for protecting the retina as well as scavenging free radicals (Akhtar
The current study investigated the antiadipogenic mechanism of krill oil from the 3T3‐L1 adipocytes. The krill oil adhered to the criteria as a food standard by showing 50.8% of the total phospholipid, 5.27% myristic acid, and 1.63% linoleic acid. The lipid accumulation that was measured in the 3T3‐L1 cells using oil red O staining was reduced up to 54% by the krill oil. The krill oil treatment reduced the adipogenic transcription factors by downregulating the sterol regulatory element binding protein 1 (SREBP1) and acetyl‐CoA carboxylase (ACC), phospho‐ACC, and AMP‐activated protein kinase (AMPK) phosphorylation. The current study confirmed that the krill oil inhibited adipogenesis by downregulating SREBP1 and ACC via the upregulation of the AMPK and nuclear factors E2‐related factor 2 (Nrf2) signaling pathway in the 3T3‐L1 adipocytes. These findings suggest that krill oil is a good source of phospholipid and phosphatidylcholine, which could be a potential natural antiobesity ingredient by inhibiting adipogenesis.
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