thioacetamide and epigallocatechin-gallate

Existing research suggests that (-)-epigallocatechin-3-gallate (EGCG), which is a natural tea catechin active substance, can protect against liver injury. However, its mechanism for hepatic encephalopathy (HE) treatment is still unclear. In this study, the role of EGCG in the amelioration of HE rats and the effect on the microbiota-gut-liver axis are mainly analyzed.. Thioacetamide (TAA) is employed to induce the HE model in rats. The results of open field test show that EGCG restores locomotor activity and exploratory behavior. Histological and biochemical results demonstrate that EGCG ameliorates brain and liver damage, decreases the expression of pro-inflammatory cytokines, and increases the activity of antioxidant enzymes. Meanwhile, EGCG modulates the Nrf2 pathway and TLR4/NF-κB pathway to mitigate TAA-induced oxidative stress and inflammatory responses. Immunohistochemistry reveals protection of the intestinal barrier by EGCG upregulating the expression of occludin and zonula occludens-1. Furthermore, serum levels of ammonia and LPS are reduced. 16S rRNA analysis shows that EGCG treatment increases the abundance of beneficial bacteria (e.g., Bifidobacterium, Lactobacillus, and Limosilactobacillus).. The above results reveal that EGCG has anti-oxidative stress and anti-inflammatory effects, and ameliorates the condition through the microbiota-gut-liver axis, with potential for the treatment of HE.

Topics: Animals; Antioxidants; Catechin; Gastrointestinal Microbiome; Hepatic Encephalopathy; Rats; RNA, Ribosomal, 16S; Tea; Thioacetamide

The aim of this study was to investigate the effect of epigallocatechin gallate (EGCG) on uncoupling protein 2 regulation in an acute liver injury-animal model.. Twenty seven male Wistar rats were divided into three groups: control group (n = 9), TAA group (n = 9): acute liver injury was induced by the intraperitoneal injection of thioacetamide (200 mg/kg) and EGCG/TAA (n = 9 rats): Epigallocatechin gallate was given two weeks prior to the induction of acute liver injury by thioacetamide. The levels of uncoupling protein 2, CRP, TNF-α and interleukins (IL) 6 and 18 were analyzed in the liver using PCR analysis.. Q-PCR analysis showed that the genetic expression of UCP2, TNF-α and CRP in the EGCG/TAA group was the least in comparison to other groups (P ≤ 0.005). The IL-6 and IL-18 were upregulated after induction of acute liver injury, but this upregulation was significantly less in the group that received epigallocatechin gallate (EGCG/TAA) compared to the TAA group. In addition, histological examination showed a reduction in hepatocyte injury in EGCG/TAA compared to the TAA group.. Epigallocatechin gallate administration prior to induction of acute liver injury down-regulates uncoupling protein 2 expression and reduces IL-6, IL-18, TNF-α and CRP.

Topics: Animals; Antioxidants; Catechin; Chemical and Drug Induced Liver Injury; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Ion Channels; Male; Mitochondrial Proteins; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction; Thioacetamide; Uncoupling Protein 2

Epigallocatechin-gallate (EGCG) claims a plethora of health benefits including protection against neoplastic diseases. Meanwhile, heparan-sulfate proteoglycans (HSPGs) have defensive role against tumour cell invasion. Therefore, the chemopreventive and hepatoprotective effects of EGCG were studied in hepatocellular carcinoma (HCC) in vivo and in vitro and compared with strong water soluble antioxidant, sodium ascorbate.. HCC was induced in SD rats by thioacetamide (200 mg/Kg). Some rats were treated with EGCG (20 mg/Kg) or sodium ascorbate (100 mg/Kg). Liver impairment was assessed by measuring serum α-fetoprotein and investigating liver sections stained with H/E. Hepatic HSPGs, syndecan-1 and matrix metalloproteinase-9 (MMP-9) were measured by ELISA. Gene expression of fibroblast growth factor (FGF)-2 was measured. Cell death was assessed by caspase-3 activity. In addition, all markers were measured in human hepatocellular carcinoma cell line (HepG2).. EGCG increased the animal survival and decreased both α-fetoprotein and HepG2 viability. In addition, EGCG ameliorated fibrosis and massive hepatic tissue breakdown. EGCG restored HSPGs and reduced expression of MMP-9, syndecan-1 and FGF-2 in-vivo and in-vitro. Sodium ascorbate showed significantly lower results than EGCG.. Besides antioxidant activity, other mechanisms are involved in the chemopreventive and hepatoprotective effects of EGCG including restoration of HSPGs receptors and inhibition of vascular invasion.

Topics: alpha-Fetoproteins; Animals; Antineoplastic Agents, Phytogenic; Antioxidants; Ascorbic Acid; Camellia sinensis; Carcinoma, Hepatocellular; Catechin; Fibroblast Growth Factor 2; Gene Expression; Hep G2 Cells; Heparan Sulfate Proteoglycans; Humans; Liver; Liver Neoplasms; Male; Matrix Metalloproteinase 9; Neoplasm Invasiveness; Phytotherapy; Plant Extracts; Rats, Sprague-Dawley; Syndecan-1; Thioacetamide