Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032 Cell Extracts Inhibit Adipogenesis in 3T3-L1 and HepG2 Cells.

Some lactic acid bacteria (LAB) and their cellular components have antiobesity effects. In this study, we evaluated the antiadipogenic effects of a mixture of two LAB-Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032-using 3T3-L1 preadipocytes and HepG2 hepatocarcinoma cells. 3T3-L1 cells treated with a 1:1 ratio of HY7601 and KY1032 during differentiation showed reduced lipid accumulation by Oil Red O staining, as well as decreased leptin secretion and mRNA expression of peroxisome proliferator-activated receptor-γ and CCAAT/enhancer binding protein-α. HY7601 and KY1032 treatment also suppressed mitochondrial biogenesis and inhibited the expression of genes encoding mitochondrial transcription factors, as well as those related to fatty acid synthesis in HepG2 cells. The antiadipogenic effects of LAB were associated with the cell membrane fraction. These results demonstrate that a mixture of two LAB (HY7601 and KY1032) inhibits adipogenesis in preadipocytes and liver cells and is a potential therapeutic strategy for the treatment of obesity.

Standardized Kaempferia parviflora Extract Inhibits Intrinsic Aging Process in Human Dermal Fibroblasts and Hairless Mice by Inhibiting Cellular Senescence and Mitochondrial Dysfunction.

Intrinsic skin aging is a complex biological phenomenon mainly caused by cellular senescence and mitochondrial dysfunction. This study evaluated the inhibitory effect of Kaempferia parviflora Wall ex. Baker ethanol extract (KPE) on H2O2-stimulated cellular senescence and mitochondrial dysfunction both in vitro and in vivo. KPE significantly increased cell growth and suppressed senescence-associated ß-galactosidase activation. KPE inhibited the expression of cell-cycle inhibitors (p53, p21, p16, and pRb) and stimulated the expression of cell-cycle activators (E2F1 and E2F2). H2O2-induced hyperactivation of the phosphatidylinositol 3-kinase/protein kinase B (AKT) signaling pathway was suppressed by KPE through regulated expression of forkhead box O3a (FoxO3a) and mammalian target of rapamycin (mTOR). KPE attenuated inflammatory mediators (interleukin-6 (IL-6), IL-8, nuclear factor kappa B (NF-κB), and cyclooxygenase-2 (COX-2)) and increased the mRNA expression of PGC-1α, ERRα, NRF1, and Tfam, which modulate mitochondrial biogenesis and function. Consequently, reduced ATP levels and increased ROS level were also reversed by KPE treatment. In hairless mice, KPE inhibited wrinkle formation, skin atrophy, and loss of elasticity by increasing the collagen and elastic fibers. The results indicate that KPE prevents intrinsic aging process in hairless mice by inhibiting cellular senescence and mitochondrial dysfunction, suggesting its potential as a natural antiaging agent.

The protective effect of Kaempferia parviflora extract on UVB-induced skin photoaging in hairless mice.

BACKGROUND: Chronic skin exposure to ultraviolet (UV) light increases reactive oxygen species (ROS) and stimulates the expression of matrix metalloproteinases (MMPs) through c-Jun and c-Fos activation. These signaling cascades induce the degradation of extracellular matrix (ECM) components, resulting in photoaging. METHODS: This study evaluated the preventive effect of the ethanol extract of Kaempferia parviflora Wall. ex. Baker (black ginger) on UVB-induced photoaging in vivo. To investigate the antiphotoaging effect of K. parviflora extract (KPE), UVB-irradiated hairless mice administered oral doses of KPE (100 or 200 mg/kg/day) for 13 weeks. RESULTS: In comparison to the UVB control group, KPE significantly prevented wrinkle formation and the loss of collagen fibers with increased type I, III, and VII collagen genes (COL1A1, COL3A1, and COL7A1). The decrease in wrinkle formation was associated with a significant reduction in the UVB-induced expression of MMP-2, MMP-3, MMP-9, and MMP-13 via the suppression of c-Jun and c-Fos activity. KPE also increased the expression of catalase, which acts as an antioxidant enzyme in skin. In addition, expression of inflammatory mediators, such as nuclear factor kappa B (NF-κB), interleukin-1ß (IL-1ß), and cyclooxygenase-2 (COX-2), was significantly reduced by KPE treatment. CONCLUSION: The results show that oral administration of KPE significantly prevents UVB-induced photoaging in hairless mice, suggesting its potential as a natural antiphotoaging material.