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10 rezultatus
Curcumol attenuates liver sinusoidal endothelial cell angiogenesis via regulating Glis-PROX1-HIF-1α in liver fibrosis.
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Curcumol may reverse early and advanced liver fibrogenesis through downregulating the uPA/uPAR pathway.
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Previous studies have suggested strong antifibrotic activity of curcumol in the liver; the underlying mechanisms of which, however, remain largely unknown. Aiming to investigate the role of curcumol in regulating early and advanced liver fibrosis, we designed a rat model with advanced liver fibrosis
Effect of Curcumol on the Fenestrae of Liver Sinusoidal Endothelial Cells Based on NF- κ B Signaling Pathway
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Objective: To study the effect of curcumol on liver sinusoidal endothelial cells (LSECs) and to analyze the mechanism of antihepatic fibrosis.
Methods: The effects of drug
Blockade of periostin-dependent migration and adhesion by curcumol via inhibition of nuclear factor kappa β signaling in hepatic stellate cells.
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Curcumol induces HSC-T6 cell death through suppression of Bcl-2: involvement of PI3K and NF-κB pathways.
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The major feature in the molecular pathogenesis of hepatic fibrosis requires maintenance of the activated hepatic stellate cells (HSCs) phenotype by both proliferation and inhibition of apoptosis. Thus, the induction of activated HSCs apoptosis has been proposed as an antifibrotic treatment
Isolation and identification of phase 1 metabolites of curcumol in rats.
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Curcumol is one of the major components of the essential oil of Curcuma wenyujin with the structure of a guaiane-type sesquiterpenoid hemiketal. It exhibits clear antitumor, antihepatic fibrosis, antioxidant, and antimicrobial activities. In this article, the metabolism of curcumol in rats was
Inhibitory activities of curzerenone, curdione, furanodienone, curcumol and germacrone on Ca 2+-activated chloride channels
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Calcium-activated chloride channels (CaCCs) as a kind of widely expressed ion channels play crucial roles in a variety of physiological regulation. TMEM16A has been identified as the molecular basis of CaCCs in numerous cell types and is considered a new drug target for many diseases. Regulating the
Curcumol induces RIPK1/RIPK3 complex-dependent necroptosis via JNK1/2-ROS signaling in hepatic stellate cells.
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It is generally recognized that hepatic fibrogenesis is an end result of increased extracellular matrix (ECM) production from the activation and proliferation of hepatic stellate cells (HSCs). An in-depth understanding of the mechanisms of HSC necroptosis might provide a new therapeutic strategy for
Effects of different ingredients of zedoary on gene expression of HSC-T6 cells.
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OBJECTIVE
To investigate the effects of four different ingredients of zedoary (Curcuma aromatica oil, Curcumol, beta-elemence, and Curcumin) on the gene expressions of hepatic stellate cells (HSCs), and to explore the molecular mechanism of zedoary against hepatic fibrosis at gene network
The main active components of Curcuma zedoaria reduces collagen deposition in human lung fibroblast via autophagy
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Disordered collagen production by fibroblasts in response to tissue injury contributes to pulmonary fibrosis (PF). Therefore, elimination of collagen deposition has becoming a potential target in PF treatment which despite standard anti-fibrosis regiment still remains challenge. Curcumin and
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