Ginsenoside F2

Ginsenoside F2 is an orally active bioactive compound that participates in the regulation of metabolism and inflammation. Ginsenoside F2 promotes the phosphorylation of AMPK and ACC, binds to PPARγ, inhibits the phosphorylation of MAPK, activates the PI3K/AKT/GSK-3β pathway, reduces GLRX expression, and regulates lipid metabolism. Ginsenoside F2 reduces ROS production and MDA levels, restores SOD activity in cells, and alleviates oxidative stress. Ginsenoside F2 induces cell apoptosis (Apoptosis) and increases the number of cleaved caspase-3-positive cells. Ginsenoside F2 reduces body weight gain, adipose tissue weight and serum lipid levels in obese mice, and activates the hepatic AMPK signaling pathway and the expression of antioxidant enzymes. Ginsenoside F2 alleviates atopic dermatitis in mice by inhibiting inflammation and reshaping the gut microbiota^[2]. Ginsenoside F2 is applicable to research related to insulin resistance, obesity, atopic dermatitis, liver cancer, glioblastoma and glioma^[1][2][3][4]. In Vitro:Ginsenoside F2 (12.5-100 μM; 2-8 days) inhibits the differentiation of 3T3-L1 cells and reduces lipid accumulation^[1].
Ginsenoside F2 (100 μM; during differentiation treatment) alters the expression of adipogenesis-related genes in MDI-induced differentiated 3T3-L1 preadipocytes, including upregulating the expression of Grin2d, Pik3cd, MMP9 and Hhip, downregulating the expression of key adipogenic genes such as PPARγ, FASN and ACC, and promoting mitochondrial biogenesis in cells^[1].
Ginsenoside F2 (100 μM; 15-180 min) activates the AMPK pathway by increasing the phosphorylation levels of AMPK and ACC in 3T3-L1 preadipocytes^[1].
Ginsenoside F2 (100 μM; 24 h) significantly reduces the viability of IR-HepG2 cells^[3].
Ginsenoside F2 (12.5-50 μM; 12 h) dose-dependently promotes glucose uptake in IR-HepG2 cells^[3].
Ginsenoside F2 (12.5-50 μM; 12 h) dose-dependently upregulates the mRNA expression of GLUT-2 and GLUT-4 in IR-HepG2 cells, and inhibits gluconeogenesis by reducing the mRNA expression of PEPCK and G6Pase^[3].
Ginsenoside F2 (12.5-50 μM; 12 h) alleviates oxidative stress in IR-HepG2 cells by reducing ROS production and MDA levels, as well as restoring SOD activity^[3].
Ginsenoside F2 (12.5-50 μM; 12 h) promotes glycogen synthesis and increases glycogen content in IR-HepG2 cells, activates the PI3K/AKT/GSK-3β signaling pathway, and elevates the phosphorylation levels of PDK1, AKT and GSK-3β^[3].
Ginsenoside F2 (12.5-50 μM; 12 h) dose-dependently inhibits the activation of the MAPK signaling pathway and suppresses the nuclear translocation of NF-κB p65 in high glucose-induced IR-HepG2 cells^[3].
Ginsenoside F2 (80 μM; 24 h) induces apoptosis and increases the number of cleaved caspase-3-positive cells in human glioblastoma cell lines U373 and Hs683^[4].
Ginsenoside F2 (80 μM; 24 h) induces DNA damage in human glioblastoma cell lines U373 and Hs683, and increases the signal intensity of γH2AX^[4].
Ginsenoside F2 (80 μM; 24 h) impairs mitochondrial function in human glioblastoma cell lines U373 and Hs683, which is specifically characterized by a significant decrease in mitochondrial membrane potential^[4].
Ginsenoside F2 (20-80 μM; 24 h) upregulates the mRNA expression of p21 and downregulates the mRNA expression of GLRX in a concentration-dependent manner in human glioblastoma cell lines U373 and Hs683^[4].
Ginsenoside F2 (20-80 μM; 24 h) inhibits mitochondrial respiration and ATP production in human glioblastoma U373 and Hs683 cells, impairs mitochondrial function, and significantly reduces mitochondrial membrane potential and intracellular NAD⁺ levels^[4].
Ginsenoside F2 (20-80 μM; 24 h) disrupts the intracellular redox balance in human glioblastoma cell lines U373 and Hs683, and reduces the GSH/GSSG ratio^[4].
Ginsenoside F2 (20-80 μM; 24 h treatment) induces energy stress in human glioblastoma cell lines U373 and Hs683, which is characterized by a concentration-dependent increase in phosphorylated AMPK levels^[4]. In Vivo:Ginsenoside F2 (50-100 mg/kg; intragastric administration; once daily for 4 consecutive weeks) reduces body weight gain, adipose tissue weight and serum lipid levels in male C57BL/6J mice with high-fat diet-induced obesity, while activating the hepatic AMPK signaling pathway and the expression of antioxidant enzymes^[1].
Ginsenoside F2 (50 mg/kg; p.o.; daily administration; 27 days) significantly alleviates Dermatophagoides farinae extract-induced atopic dermatitis in BALB/c mice by suppressing cutaneous and systemic inflammation, reshaping the gut microbiota to enrich propionate-producing bacteria, and increasing propionate levels in feces and serum^[2].