Maltol (3-hydroxy-2-methyl-4-pyrone) is used widely as a food and cosmetic supplement, and it has antioxidant and anti-inflammatory activities. Inflammasome causes the maturation and secretion of interleukin (IL)-1β and -18 through the activation of caspase-1 (Casp1), which contributes to various inflammatory diseases. This study examined the effects of maltol on the inflammasome activation in macrophages and mice. Lipopolysaccharide (LPS)-primed macrophages were treated with a trigger of NLRP3, NLRC4, AIM2, or non-canonical (NC) inflammasomes in the presence of maltol. The secretion of IL-1β and IL-18 and the cleavage of Casp1 were analyzed as indices of inflammasome activation. Mice were injected with LPS and an NLRP3 trigger with or without maltol, and the peritoneal IL-1β secretions were observed. The effects of maltol on reactive oxygen species (ROS) production and Casp1 activity were analyzed to determine the mechanism. Maltol inhibited the activation of NLRP3 and NC inflammasomes, but it did not alter the other inflammasomes. Maltol also attenuated IL-1β secretion resulting from the inflammasome activation in mice. The anti-inflammatory mechanism of maltol was revealed by the inhibition of ROS production and Casp1 activity. Maltol is suggested to be promising as a anti-inflammasome molecule.

Background: This study was conducted to assess the efficacy and safety of Red Ginseng Extract Powder (RGEP) (KGC05pg; Korea Ginseng Corporation, Daejeon, Korea) in achieving glycemic control in prediabetic Korean adults. Methods: The patients of the RGEP group (n = 49) and those of the placebo group (n = 49) were orally given 2 tablets of RGEP and its matching placebo, respectively, at a dose of 500 mg/day twice daily in the morning and the evening within 30 min after meal during a 12-week treatment period. The patients were assessed for glycemic control parameters, such as fasting blood glucose levels, 30-, 60-, 90-, and 120-min blood glucose levels on an oral glucose tolerance test, Hb1Ac levels and glucose area under the curve, insulin resistance parameters, such as homeostasis model assessment of insulin resistance, c-peptide and insulinogenic index, and hormone parameters, such as glucagon, adiponectin and glucagon-like peptide-1. Moreover, the patients were also assessed for time-dependent changes in dipeptidyl peptidase-4 levels. Finally, the patients were also assessed for incidences of treatment-emergent adverse events and serious adverse events. Results: There were significant differences in changes in fasting blood glucose and 30-, 60-, 90-, and 120-min blood glucose levels on an oral glucose tolerance test, Hb1Ac levels, glucose area under the curve, homeostasis model assessment of insulin resistance, c-peptide levels and insulinogenic index, glucagon, adiponectin, and glucagon-like peptide-1 levels at 12 weeks from baseline between the 2 groups (P < .05). There was a significant time-dependent decrease in dipeptidyl peptidase-4 levels in the RGEP group (P = .001). There were no cases of treatment-emergent adverse events and serious adverse events in each treatment arm. Conclusion: RGEP might be effective in achieving glycemic control in prediabetic Korean adults.

In this study, we determined the probiotic properties and safety of Limosilactobacillus reuteri KGC1901 isolated from Korean Panax ginseng root. This strain was identified based on its 16s rRNA sequence, and the absence of genes related to antibiotic resistance and virulence was confirmed through whole genome analysis in terms of safety. Moreover, this strain had no antibiotic resistance to eight antibiotics as proposed by the European Food Safety Authority, did not show hemolytic activity on blood agar, and did not produce biogenic amines. L. reuteri KGC1901 also showed the capability to survive at low pH and in presence of bile salts and sufficiently adhered to HT-29 cells and mucin. The adhesion ability to HT-29 was confirmed by immunofluorescence staining. These results indicated the excellent viability of L. reuteri KGC1901 in the human gastrointestinal tract. Additionally, L. reuteri KGC1901 had antimicrobial activity against Clostridium difficile, and the presence of the reuterin (3-HPA) biosynthetic gene cluster in the genome was revealed. Furthermore, the cell-free supernatant of KGC1901 had DPPH scavenging activity and reduced the nitric oxide production in LPS-stimulated RAW 264.7 cells. Based on these results, it was confirmed that L. reuteri KGC1901 derived from ginseng has sufficient potential to be used as a probiotic.

Skin microbiota is important for maintenance of skin homeostasis; however, its disturbance may cause an increase in pathogenic microorganisms. Therefore, we aimed to develop a red ginseng formulation that can selectively promote beneficial bacteria. The effects of red ginseng formulation on microorganism growth were analyzed by comparing the growth rates of Staphylococcus aureus, S. epidermidis, and Cutibacterium acnes. Various preservatives mixed with red ginseng formulation were evaluated to determine the ideal composition for selective growth promotion of S. epidermidis. Red ginseng formulation with selected preservative was loaded into a biocompatible polymer mixture and applied to the faces of 20 female subjects in the clinical trial to observe changes in the skin microbiome. Red ginseng formulation promoted the growth of S. aureus and S. epidermidis compared to fructooligosaccharide. When 1,2-hexanediol was applied with red ginseng formulation, only S. epidermidis showed selective growth. The analysis of the release rates of ginsenoside-Rg1 and -Re revealed that the exact content of Pluronic F-127 was around 11%. The application of hydrogel resulted in a decrease in C. acnes in all subjects. In subjects with low levels of S. epidermidis, the distribution of S. epidermidis was significantly increased with the application of hydrogel formulation and total microbial species of subjects decreased by 50% during the clinical trial. We confirmed that red ginseng formulation with 1,2-hexanediol can help maintain skin homeostasis through improvement of skin microbiome.

Etoposide, an anticancer drug that inhibits topoisomerase II, is commonly used in combination chemotherapy. However, the impact of O‐GlcNAcylation regulation on etoposide's anticancer effects has rarely been investigated. This study evaluated the effect of etoposide on cellular O‐GlcNAcylation and whether modulating this process enhances etoposide‐induced apoptosis. O‐GlcNAc expression was measured after 24 h of etoposide treatment, and the effect of O‐GlcNAc transferase (OGT) inhibition by OSMI‐1 on etoposide's anticancer activity in HepG2 human liver cancer cells was quantitatively analyzed. Additionally, molecular analyses were used to confirm that the observed effects were mediated by p53‐induced apoptosis. Etoposide reduced O‐GlcNAcylation in a dose‐dependent manner without directly interacting with OGT. Cotreatment with 20 μm of OSMI‐1 lowered the IC₅₀ value for cell viability by approximately 1.64‐fold to 60.68 μm and increased the EC₅₀ value for cytotoxicity by around 4.07‐fold to 43.41 μm. Furthermore, this synergistic effect was linked to the activation of the p53/caspase‐3/PARP1 pathway. These findings suggest that downregulating O‐GlcNAcylation may enhance the efficacy of etoposide‐based chemotherapy and help overcome tumor resistance.