likviriton has been researched along with Fibrosis* in 3 studies
3 other study(ies) available for likviriton and Fibrosis
| Article | Year |
|---|---|
Liquiritin Protects Against Cardiac Fibrosis After Myocardial Fibrosis After Myocardial Infarction by Inhibiting CCL5 Expression and the NF-κB Signaling Pathway [Letter].
Topics: Chemokine CCL5; Fibrosis; Humans; Myocardial Infarction; Myocardium; NF-kappa B; Signal Transduction | 2023 |
Liquiritinapioside - A mineralocorticoid-like substance from liquorice.
Topics: Animals; Cell Line; China; Collagen Type I; Fibrosis; Flavanones; Glucosides; Glycyrrhiza; Humans; MAP Kinase Signaling System; Mineralocorticoids; Myocardium; Plant Extracts; Receptors, Mineralocorticoid; Signal Transduction; Terpenes; Transforming Growth Factor beta1 | 2019 |
The protective role of liquiritin in high fructose-induced myocardial fibrosis via inhibiting NF-κB and MAPK signaling pathway.
Diabetic cardiomyopathy has been known as an important complication of diabetes and characterized by persistent diastolic dysfunction, resulting in myocardial fibrosis, which is associated inflammatory response and oxidative stress. Liquiritin is a major constituent of Glycyrrhiza Radix, possessing various pharmacological activities and exhibiting various positive biological effects, including anti-cancer, anti-oxidative and neuroprotective effects. Here, we investigated the anti-inflammatory properties and protective effects of lquiritin in high fructose-induced mice and cardiomyocytes to clarify the potential mechanism. The mice were divided into the control mice, 30% high fructose-induced mice, 10mg/kg liquiritin-treaed mice after fructose feeding and 20mg/kg liquiritin-treaed mice after fructose feeding. Liquiritin effectively reduced the lipid accumulation and insulin resistance induced by fructose feeding. In comparison to high fructose-feeding control mice, liquiritin-treated mice developed less myocardial fibrosis with lower expression of Collagen type I, Collagen type II and alpha smooth muscle-actin (α-SMA). In addition, liquiritin significantly reduced the inflammatory cytokine release and NF-κB phosphorylation through IKKα/IκBα signaling pathway suppression. Further, Mitogen-activated protein kinases (MAPKs), including p38, ERK1/2 and JNK, was up-regulated for fructose stimulation, which was inactivated by liquiritin treatment in vivo and in vitro studies. Our data indicates that liquiritin has a protective effect against high fructose-induced myocardial fibrosis via suppression of NF-κB and MAPKs signaling pathways, and liquiritin may be a promising candidate for diabetes-related myocardial fibrosis treatment. Topics: Animals; Cell Survival; Collagen; Down-Regulation; Feeding Behavior; Fibrosis; Flavanones; Fructose; Glucosides; Inflammation; Insulin Resistance; Lipid Metabolism; Male; MAP Kinase Signaling System; Mice, Inbred C57BL; Mitogen-Activated Protein Kinases; Myocardium; Myocytes, Cardiac; NF-kappa B; Protective Agents | 2016 |