GC/MS-Based Metabolomics Approach to Evaluate the Effect of Jackyakgamcho-Tang on Acute Colitis.

The objective of this study was to examine the effects of Jackyakgamcho-tang (JGT) on acute colitis. GC/MS-based metabolomics and NGS-based metagenomics were applied to investigate the alteration of metabolites and microbiota in an acute colitis model. The severity of acute colitis symptoms was alleviated by JGT treatment. Induction of colitis and JGT treatment changed compositions of gut microbiota and inflammatory cytokine levels (TNF-α and IL-6). They also substantially change metabolites (i.e., lactic acid, linoleic acid, monostearin, and palmitoylglycerol). In addition, some clear correlations were observed among metabolites, cytokine, and microbiota. This study highlights the applicability of metabolomics and metagenomics study for evaluating anti-inflammatory effects of a new functional herbal medicine as a therapeutic agent for acute colitis.

KCHO-1, a Novel Antineuroinflammatory Agent, Inhibits Lipopolysaccharide-Induced Neuroinflammatory Responses through Nrf2-Mediated Heme Oxygenase-1 Expression in Mouse BV2 Microglia Cells.

The brain is vulnerable to oxidative stress and inflammation that can occur as a result of aging or neurodegenerative diseases. Our work has sought to identify natural products that regulate heme oxygenase (HO)-1 and to determine their mechanism of action in neurodegenerative diseases. KCHO-1 is a novel herbal therapeutic containing 30% ethanol (EtOH) extracts from nine plants. In this study, we investigated the antineuroinflammatory effects of KCHO-1 in lipopolysaccharide- (LPS-) treated mouse BV2 microglia. KCHO-1 inhibited the protein expression of inducible nitric oxide synthase (iNOS), iNOS-derived nitric oxide (NO), cyclooxygenase- (COX-) 2, and COX-2-derived prostaglandin E2 (PGE2) in LPS-stimulated BV2 microglia. It also reduced tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-6 production. This effect was correlated with the suppression of inhibitor of nuclear factor kappa B-α (IκB-α) phosphorylation and degradation and nuclear factor kappa B (NF-κB) translocation and DNA binding. Additionally, KCHO-1 upregulated HO-1 expression by promoting nuclear translocation of nuclear factor E2-related factor 2 (Nrf2) in mouse BV2 microglia. Tin protoporphyrin (SnPP), an HO activity inhibitor, was used to verify the inhibitory effects of KCHO-1 on proinflammatory mediators and proteins associated with HO-1 expression. Our data suggest that KCHO-1 has therapeutic potential in neurodegenerative diseases caused by neuroinflammation.