monascin has been researched along with Liver-Cirrhosis* in 2 studies
2 other study(ies) available for monascin and Liver-Cirrhosis
| Article | Year |
|---|---|
Ankaflavin and Monascin Induce Apoptosis in Activated Hepatic Stellate Cells through Suppression of the Akt/NF-κB/p38 Signaling Pathway.
The increased proliferation of activated hepatic stellate cells (HSCs) is associated with hepatic fibrosis and excessive extracellular matrix (ECM)-protein production. We examined the inhibitory effects of the Monascus purpureus-fermented metabolites, ankaflavin and monascin (15 and 30 μM), on the Akt/nuclear factor (NF)-κB and p38 mitogen-activated protein kinase (MAPK) signaling pathways in HSC-T6 (activated hepatic stellate cell line). Ankaflavin and monascin (30 μM) induced apoptosis and significantly inhibited cell growth (cell viabilities: 80.2 ± 5.43% and 62.8 ± 8.20%, respectively, versus control cells; P < 0.05). Apoptosis and G1 phase arrest (G1 phase percentages: 76.1 ± 2.85% and 79.9 ± 1.80%, respectively, versus control cells 65.9 ± 4.94%; P < 0.05) correlated with increased p53 and p21 levels and caspase 3 activity and decreased cyclin D1 and Bcl-2-family protein levels (P < 0.05, all cases). The apoptotic effects of ankaflavin and monascin were HSC-T6-specific, suggesting their potential in treating liver fibrosis. Topics: Animals; Apoptosis; Cell Proliferation; Cell Survival; Cells, Cultured; Down-Regulation; Flavins; Hepatic Stellate Cells; Heterocyclic Compounds, 3-Ring; Humans; Liver Cirrhosis; Male; Monascus; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Plant Extracts; Proto-Oncogene Proteins c-akt; Rats; Signal Transduction | 2016 |
Peroxisome proliferator-activated receptor-γ activators monascin and rosiglitazone attenuate carboxymethyllysine-induced fibrosis in hepatic stellate cells through regulating the oxidative stress pathway but independent of the receptor for advanced glycat
Advanced glycation end products (AGEs) signaling through its receptors (RAGE) results in an increase in reactive oxygen species (ROS) and is thought to contribute to hepatic fibrosis via hyperglycemia. Carboxymethyllysine (CML) is a key AGE, with highly reactive dicarbonyl metabolites. We investigated the inhibitory effect of Monascus -fermented metabolite monascin and rosiglitazone on CML-induced RAGE signaling in hepatic stellate cells (HSCs) and its resulting antihepatic fibrosis activity. We found that monascin and rosiglitazone upregulated peroxisome proliferator-activated receptor-γ (PPAR-γ) to attenuate α-smooth muscle actin (SMA) and ROS generation in CML-treated HSCs in a RAGE activation-independent pathway. Therefore, monascin may delay or inhibit the progression of liver fibrosis through the activation of PPAR-γ and might prove to be a major antifibrotic mechanism to prevent liver disease. Topics: Animals; Anti-Inflammatory Agents; beta-Glucans; Cells, Cultured; Hepatic Stellate Cells; Heterocyclic Compounds, 3-Ring; Liver Cirrhosis; Lysine; Male; Mice; Oxidative Stress; PPAR gamma; Receptor for Advanced Glycation End Products; Receptors, Immunologic; RNA, Small Interfering; Rosiglitazone; Signal Transduction; Thiazolidinediones; Transfection | 2013 |