White crystalline powder
philligenin/sylvatesmin/Phillygenol/4-[(1S,3aR,4R,6aR)-4-(3,4-Dimethoxyphenyl)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-2-methoxyphenol/(+)-Phillygenin/Epipinoresinol methyl ether/Phenol, 4-[(1S,3aR,4R,6aR)-4-(3,4-dimethoxyphenyl)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-2-methoxy-/phylligenin/Phillygenin
Phillygenin is an active ingredient from Forsythia with many medicinal properties, such as antioxidant, reducing blood lipid, inhibition of low density lipoprotein oxidation.In vitro : 1) Phillygenin shows a greater inhibition on mouse B16 melanoma cells potential than vincristine.2) phillygenin had notable scavenging activity against DPPH, ABTS radicals, as well as potent reducing power in FRAP assay.In vivo: The reference for rat is 5.6 mg/m l ( i.v).
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Phillygenin is a bioactive intergradient in Osmanthus fragrans, a well-known food additive and Chinese traditional medicine. This study was to investigate the hepatoprotective effects and pharmacokinetics of phillygenin. The hepatoprotective effect of phillygenin was assessed in carbon tetrachloride- (CCl4-) intoxicated mice by monitoring levels of serum and tissue biomarkers. The pharmacokinetics of phillygenin was evaluated in the mouse after oral (po, 24 mg / kg) or intravenous (iv, 12 mg/kg) administration. Results showed that phillygenin has a great hepatoprotective effect on CCl4-induced liver injury in mice owing to its antioxidant activity and inhibition on cytochrome P450 2E1(CYP2E1). After oral administration, phillygenin was efficiently absorbed with the oral bioavailability of 56.4%. Two metabolites, hydroxylated and dimethylated phillygenin, were identified in mouse urine. These results suggested that phillygenin could be explored as new and potential natural antioxidants and hepatoprotective agents.
Evaluation of the Pharmacokinetics and Hepatoprotective Effects of Phillygenin in Mouse.
Song W1,2, Wu J3, Yu L2, Peng Z1.
2018 Aug 23
BACKGROUND Esophageal cancer causes considerable mortality and is ranked as the 6th most prevalent type of cancer across the world. At present, there is no effective esophageal cancer chemotherapy without adverse effects. Moreover, emergence of drug resistance among cancer is another obstacle in the treatment of esophageal cancer. Novel molecules of plant origin may prove beneficial in the development of chemotherapy for esophageal carcinoma. In this study we examined the anticancer effects of phillygenin against the vindesine-resistant esophageal cancer cell line SH-1-V1. MATERIAL AND METHODS The proliferation rate of SH-1-V1 cells was determined by WST-1 assay. Apoptosis was confirmed by propidium iodide (PI) staining. Cell cycle analysis, ROS, and MMP determination were performed by flow cytometery. Protein expression was assessed by Western blot analysis. RESULTS We found that phillygenin inhibited the growth of SH-1-V1 cells and exhibited an IC50 of 6 µM. Investigation of the underlying mechanism revealed that phillygenin triggered apoptotic cell death of the SH-1-V1 cells, which was also associated with enhancement of Bax expression and decreased expression of Bcl-2. Moreover, the expression of cleaved caspase 3 and 9 also increased upon phillygenin treatment. Phillygenin also caused a significant increase in ROS production, concomitant with decreased MMP levels. Phillygenin also caused arrest of cells in the G2/M phase of the cell cycle. In vivo evaluation of phillygenin revealed that it can inhibit tumor weight and volume, suggesting the anticancer potential of phillygenin. CONCLUSIONS In brief, phillygenin inhibited in vitro and in vivo cancer cell growth in drug-resistant human esophageal cancer cells, and these effects were mediated via apoptosis, ROS generation, mitochondrial membrane potential loss, and activation of the NF-kB signalling pathway.
Phillygenin Exerts In Vitro and In Vivo Antitumor Effects in Drug-Resistant Human Esophageal Cancer Cells by Inducing Mitochondrial-Mediated Apoptosis, ROS Generation, and Inhibition of the Nuclear Factor kappa B NF-κB Signalling Pathway.
He J1, Wei W2, Yang Q1, Wang Y1.
2019 Jan 25
Context: Phillygenin (PHI) is an intestinal metabolite of phillyrin from the genus Forsythia. Although the regulatory activity of Forsythia on immune system has been investigated, the effect of PHI on activated lymphocytes is poorly understood. Objective: This study was aimed to discuss the possible anti-inflammation potential of PHI on mitogen-activated stimulated lymphocytes in vitro. Methods: Mice spleen lymphocytes were incubated with PHI for 4 h, and then stimulated with concanavalin A (Con A) or phorbol 12-myristate 13-acetate/ionomycin (PMA + Ion). Cell viability was assayed by cell counting kit-8 (CCK-8). The expression of CD69 and CD25, proliferation, cell cycle, intracellular Ca2+ concentration, apoptosis, mitochondrial inner membrane potential (ΔΨm), mitochondrial permeability transition (MPT), interleukin-2 (IL-2), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) were analyzed by flow cytometry. The expression of cyclin B1, cyclin D1, Cyclin E, and the phosphorylation of c-jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (Erk1/2) and p38 were assayed by western blotting. Results: The results showed that PHI inhibited the proliferation of Con A-activated lymphocytes and induced a G0/G1 phase arrest by suppressing cyclin D1 and cyclin E. Meanwhile, PHI antagonized Con A-induced T cells activation through blocking intracellular Ca2+ overload and suppressing the phosphorylation of JNK and Erk1/2. Both Con A and PMA + Ion-induced secretion of IL-2, IFN-γ, and TNF-α were attenuated by PHI. PHI enhanced Con A-induced lymphocytes apoptosis through decreasing ΔΨm and increasing MPT. Conclusion: These results suggest that PHI exhibits its anti-inflammatory activity through modulating multiple cellular behaviors, leading to the suppression of the adaptive immune response.
Phillygenin; T lymphocytes; activation; anti-inflammation; proliferation
Phillygenin exhibits anti-inflammatory activity through modulating multiple cellular behaviors of mouse lymphocytes.
Du B1,2,3, Zhang L1, Sun Y1, Zhang G1,2, Yao J1,2,3, Jiang M1,2,3, Pan L1,2,3, Sun C1,2,3.