Korean ginseng (Panax ginseng) is a traditional herbal supplement known to have a variety of pharmacological activities. A smart farm system could provide potential standardization of ginseng seedlings after investigating plant metabolic responses to various parameters in order to design optimal conditions. This research was performed to investigate the effect of smart-farmed ginseng on memory improvement in a scopolamine-induced memory deficit mouse model and an LPS-induced microglial cell model. A smart farming system was applied to culture ginseng. The administration of its extract (S2 extract) under specific culture conditions significantly attenuated cognitive and spatial memory deficits by regulating AKT/ERK/CREB signaling, as well as the cortical inflammation associated with suppression of COX-2 and NLRP3 induced by scopolamine. In addition, S2 extract improved the activation of iNOS and COX-2, and the secretion of NO in LPS-induced BV-2 microglia. Based on the HPLC fingerprint and in vitro data, ginsenosides Rb2 and Rd were found to be the main contributors to the anti-inflammatory effects of the S2 extract. Our findings suggest that integrating a smart farm system may enhance the metabolic productivity of ginseng and provides evidence of its potential impact on natural bioactive compounds of medicinal plants with beneficial qualities, such as ginsenosides Rb2 and Rd.

Sinapic acid (SA) is a phenolic acid that is widely found in fruits and vegetables, which has various bioactivities, such as antidiabetic, anti-in ammatory, anticancer and anxiolytic functions. Overactivated microglial cells play a major role in the development of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. The objective of this study was to investigate the effect and mechanism of sinapic acid in microglia-derived neuroin ammatory models. Our results demonstrated that SA inhibited production of the nitric oxide (NO) pro-in ammatory factor, induced nitric oxide synthase (iNOS), induced interleukin (IL)-6 and enhanced the release of IL-10 in a dose-dependent manner. Subsequently, a mechanistic study revealed that SA remarkably attenuated the phosphorylation of AKT and MAPK cascades in LPS-induced microglia. Consistently, administration of SA regulated the production of in ammation-related cytokines and inhibited the phosphorylation of MAPK cascades and Akt in the mouse cerebral cortex. These results suggested that SA may offer a possible treatment for antiin ammatory activity by targeting the AKT/MAPK signaling pathway.