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Research Article: Luteolin Alleviates Liver Fibrosis in Rat Hepatic Stellate Cell HSC-T: A Proteomic Analysis

Date Published: 2023-06-17

Abstract:
Liver fibrosis is caused by chronic liver disease and can worsen into hepatic cirrhosis or even hepatocellular carcinoma (HCC). Liver transplantation is the only feasible way to treat advanced stages liver fibrosis patients. Thus, there is an urgent need for new therapeutic agents and treatment strategies. The primary mechanism of fibrosis depends on hepatic stellate cells (HSCs), which become fibrogenic myofibroblasts during injury and are closely linked to the development of the novel drug targets. Quiescent HSCs exit the Space of Disse (sinusoidal endothelial cell layer), which includes –% of the liver, and may help to regulate the hepatic vascular system. While transient HSCs are beneficial to liver reconstruction following brachychronic injury, unremitting activation associated with chronic injury can cause liver fibrosis. Activated HSCs promote severe cell propagation and tremendous variation in their stellate morphology, together with lipid deposition, imbalanced degradation of the extracellular matrix (ECM), and increased production of the HSC-specific marker protein, alpha-smooth muscle actin (?-SMA)., Activated HSCs also induce proinflammatory and profibrotic factors generated by inflammatory cells, including transforming growth factor ? (TGF-?). TGF-? can also activate HSCs, inducing an autocrine-active feedback circuit which exacerbates liver fibrogenesis., To date, the only feasible systemic chemotherapeutic agent that increases the survival of advanced-stage HCC patients is the multi-tyrosine kinase inhibitor, sorafenib.

Introduction:
Liver fibrosis is caused by chronic liver disease and can worsen into hepatic cirrhosis or even hepatocellular carcinoma (HCC). Liver transplantation is the only feasible way to treat advanced stages liver fibrosis patients. Thus, there is an urgent need for new therapeutic agents and treatment strategies. The primary mechanism of fibrosis depends on hepatic stellate cells (HSCs), which become fibrogenic myofibroblasts during injury and are closely linked to the development of the novel drug targets. Quiescent…

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