Expression of Toll‐like receptor 4 in rat liver during the course of carbon tetrachloride‐induced liver injury

Abstract

The gene expression of TLR4 was upregulated during the course of CCl(4)-induced liver injury, which is associated with the degree of liver injury and Kupffer cell activation. The gut-derived endotoxin may be involved in the upregulation of TLR4 expression.

Increased susceptibility to exacerbated liver injury in hypercholesterolemic ApoE-deficient mice: potential involvement of oxysterols

“…In this regard, compared with controls, ApoE-deficient mice showed increased inflammation at the sixth week of treatment, whereas increased fibrosis, assessed by Sirius red staining and ␣-SMA, was detected 2 wk later, at the eighth week of treatment. A similar peak in the inflammatory response at the sixth week of treatment followed by a decline at the eighth week, when fibrosis is more evident, has previously been described (18). This temporal dissociation is consistent with the natural course of liver disease (1) and could reflect active inflammation and necrosis accompanied by diffuse deposition of extracellular matrix in the sinusoids in early stages of the disease, followed by the replacement of the damaged tissue by extracellular matrix proteins that begin to form fibrotic tracts and bridge fibrosis at more advanced stages.…”

Innate immune reactivity of the liver in rats fed a cholinedeficient L-amino-acid-defined diet

“…The intake of alcohol facilitates the permeability of endotoxin from the gut to the portal vein, and the increased concentration of endotoxin in the portal vein leads to Kupffer cell activation via TLR4, with consequent increases in the liver expression of TNF-α, progression of inflammation, and fibrosis of the liver [24] . In the experimental chronic liver injury model, the expression of TLR4 in isolated Kupffer cells increases with progression of liver injury [25] , suggesting a correlation between inflammation and expression of The basic TNF-α production of Kupffer cells isolated from 4-and 8-wk CDAA-fed rats was equal to that of the control rats. After LPS stimulation, the TNF-α production of the control rats was significantly higher than the basic control levels, and that of the 4-and 8-wk CDAA-fed rats was significantly higher than that of the control rats.…”

A Standardized Aqueous Extract ofAnoectochilus formosanusAmeliorated Thioacetamide-Induced Liver Fibrosis in Mice: The Role of Kupffer Cells

“…18) TNF-is known to be one of the earliest events in hepatic inflammation, triggering a wound-healing response that includes fibrogenesis. 16) This proinflammatory activity resembles one of the cascades initiated by the binding of TNF-to its receptors TNF-R1. 28) Since the level of TNF-mRNA in the liver is changeable, 29) TNFR1 mRNA expression was monitored instead in this study.…”

“…2229; Fax: +886-4-22053764; E-mail: wclin@mail.cmu.edu.tw Abbreviations: ALT, alanine aminotransferase; LPS, lipopolysaccharide; SAEAF, standardized aqueous extract of Anoectochilus formosanus; TAA, thioacetamide; TLR4, Toll-like receptor 4; TNF-, tumor necrosis factor ; TNFR1, TNF receptor 1 through activation of TLR-4 in Kupffer cells, which play an essential role in the development of liver fibrosis. 16) In screening tests, we observed an ability of kinsenoside to inhibit LPS-induced TNF-production in Kupffer cells. Hence, in order to elucidate the role of Kupffer cells in the anti-fibrotic effect of SAEAF.…”