(-)-Asarinin

(-)-Asarinin is a tetrahydrofurofurano lignan with various biological activities. (-)-Asarinin induces apoptosis in cancer cells. (-)-Asarinin promotes mitochondrial ROS accumulation, inhibits the STAT3 signaling pathway and induces apoptosis in precancerous cells. (-)-Asarinin is a Src family kinase inhibitor that suppresses mast cell activation. (-)-Asarinin is a non-competitive Δ5-desaturase inhibitor with a K_i of 0.28 mM. (-)-Asarinin possesses pain relief, anti-viral, anti-allergic and anti-tuberculous bacilli, and anti-tumor effects^[1][2][3][4]. In Vitro:(-)-Asarinin (20-140 μM; 24-48 h) significantly inhibits the viability of MC cells, a human gastric precancerous lesion cell line, in a dose-dependent manner with an IC₅₀ value of 140 μM, while having no significant inhibitory effect on the viability of normal gastric epithelial cells GES-1^[1].
(-)-Asarinin (80-140 μM; 24-48 h) inhibits the clonogenic ability of MC cells. (-)-Asarinin significantly reduces the migration and invasion abilities of MC cells^[1].
(-)-Asarinin (80-140 μM; 24 h) significantly induces apoptosis and induces G₀/G₁ phase arrest in MC cells. (-)-Asarinin downregulates the expression of cell cycle-related proteins cyclin E1 and cyclin E2 and upregulates the expression of apoptosis - related proteins cleaved caspase 3 and cleaved PARP in MC cells^[1].
(-)-Asarinin (80-140 μM; 24 h) causes mitochondrial damage, reduces mitochondrial membrane potential, decreases ATP production, and increases mitochondrial ROS accumulation in MC cells^[1].
(-)-Asarinin (80-140 μM;) inhibits the expression of STAT3-pathway-related proteins p-STAT3, Bcl-2, and cyclin D1 in MC cells in the STAT3 pathway-related experiments^[1].
(-)-Asarinin (0-90 μM; 48h) induces apoptotic cell death and activates caspase-3, caspase-8, and caspase-9 in human ovarian cancer cells (A2780 and SKOV3)^[2].
(-)-Asarinin (25 μM; for 30 min) significantly reduces the calcium flux in sensitized LAD2 cells in the calcium mobilization assay^[3]. (-)-Asarinin (50 μM; for 20 min) significantly inhibits the release of β - hexosaminidase in sensitized LAD2 cells in the β-hexosaminidase release assay, with an IC₅₀ value of 35.26 μM^[3].
(-)-Asarinin (50 μM; for 20 min) significantly inhibits the release of histamine in sensitized LAD2 cells in the histamine release assay^[3].
(-)-Asarinin significantly reduces the concentrations of TNF- α, MCP-1, IL-4, and IL-5 in sensitized LAD2 cells in the cytokine release assay^[3].
(-)-Asarinin (100 μM; 6 h) inhibits the phosphorylation of Src family kinases such as Lyn and Fyn and downregulates the phosphorylation levels of downstream signals such as PLC-γ1, p38α, and Akt in LAD2 cells in the phosphorylated kinase analysis experiment^[3]. In Vivo:(-)-Asarinin (5-20 mg/kg; gavage; once daily; 16 weeks) improves the morphology of gastric mucosal glands, alleviate intestinal metaplasia, inhibit the STAT3 pathway, promote ROS accumulation, and induce apoptosis of gastric mucosal cells in the N-Nitroso-N-methylurea (MNU) (HY-34758)-induced mouse model of gastric precancerous lesions^[1].
(-)-Asarinin (5.0 mg/kg; oral administration; before intranasal OVA challenge) significantly inhibits the allergic reaction, reduces paw swelling and Evans blue exudation in mice, and decreases the degree of mast cell degranulation in the skin in the OVA-induced passive cutaneous anaphylaxis mouse model^[3].
(-)-Asarinin (2.50 mg/kg; oral administration) reduces the concentrations of histamine, TNF-α, MCP-1, IL-4, and IL-5 in the serum of mice in the OVA - induced systemic anaphylaxis mouse model<^[3].
(-)-Asarinin (5.0 mg/kg; oral administration; once daily; from day 21-28) significantly inhibits the scratching and sneezing responses of mice, reduces the concentrations of histamine, total IgE, and IL-4 in the serum of mice, and alleviates the inflammatory infiltration and thickening of the nasal mucosa in the OVA-induced allergic rhinitis mouse model^[3].
(-)-Asarinin (2.5 mg/kg, 5.0 mg/kg, 10 mg/kg; oral administration) inhibits paw swelling and Evans blue exudation in mice and reduces the concentrations of histamine, TNF-α, MCP-1, and IL-8 in the serum in the C48/80-induced allergic reaction mouse model^[3].
C57BL/6 mice (male, 18-22 g), OVA-induced passive cutaneous anaphylaxis model³ 5.0 mg/kg Oral administration Significantly suppressed passive cutaneous anaphylaxis (PCA) in mice, reduced the degree of swelling and Evens blue exudation of mice paw, and decreased the degree of degranulation of MCs in skin. C57BL/6 mice (male, 18-22 g), OVA-induced passive cutaneous anaphylaxis model³ 2.50 mg/kg Oral administration Significantly reduced the concentration of histamine, TNF-α, MCP-1, IL-4 and IL-5 in mice serum. C57BL/6 mice (male, 18-22 g), OVA-induced passive cutaneous anaphylaxis model³ 5.0 mg/kg Oral administration, once daily, from day 21 - 28 Significantly inhibited the scratching and sneezing response of mice, reduced the concentration of histamine, total IgE, and IL - 4 in mice serum, and attenuated the inflammatory infiltrates and nasal mucosa incrassation in the AR mice. C57BL/6 mice (male, 18-22 g), C48/80-induced allergic reaction model³ 2.5 mg/kg, 5.0 mg/kg, 10 mg/kg Oral administration Reduced C48/80-induced paw swelling and Evens blue exudation, and decreased the concentration of histamine, TNF-α, MCP-1 and IL-8 in mice serum.