Epigallocatechin gallate attenuates fibrosis, oxidative stress, and inflammation in non-alcoholic fatty liver disease rat model through TGF/SMAD, PI3 K/Akt/FoxO1, and NF-kappa B pathways

Xiao, Jia; Ho, Chi Tat; Liong, Emily C.; Nanji, Amin A.; Leung, Tung Ming; Lau, Thomas Y.H.; Fung, Man Lung; Tipoe, George L.

doi:10.1007/s00394-013-0516-8

Cited by 171 publications

(139 citation statements)

References 42 publications

Supporting

Mentioning

129

Contrasting

Order By: Relevance

“…In this investigation, to imitate the clinical scenario of RA, CIA was induced in Lewis rats and subsequently, the anti-arthritic potency of Camellia sinensis stew was assessed in mentioned experimental model. This beverage is being used for many years and possesses antioxidant activities, anti-inflammatory, anti-apoptotic properties and protective effects in autoimmune animal models [11][12][13][14][15].…”

Section: Discussionmentioning

confidence: 99%

Camellia Sinensis Modulates Telomerase in Collagen-Induced Arthritis

Jalali

Saadat

2017

Zahedan J Res Med Sci

View full text Add to dashboard Cite

Background: Rheumatoid arthritis is a chronic inflammatory disease with undefined pathogenesis. Some evidence suggests that telomerase is involved in the pathogenesis of this disease. This study was done to evaluate the therapeutic potency of Camellia sinensis stew (CSS) which rich in polyphenolic compounds with anti-inflammatory properties in experimental model of rheumatoid arthritis. Methods: In this experimental study, collagen-induced arthritis (CIA) was induced by immunization of Lewis rats. The paws and knees were then removed for histopathology analysis. Moreover, Roentgenogram analysis of normal and arthritic hind paws was performed. Synovial cell harvested from biopsies of synovial tissue were used for measuring telomerase activity. The results were analyzed using SPSS version 16 software. Results: Our data showed that CSS induced a significant reduction in paw edema. Histopathological findings showed reduced inflammatory responses and bone erosion in joints of treated rats. Moreover, CSS showed a significant reduction of telomerase activity compares with control group. Conclusions: Our findings revealed that CSS should be considered as a therapeutic agent in experimental model of rheumatoid arthritis based on its telomerase activity suppression.

show abstract

Section: Discussionmentioning

confidence: 99%

Camellia Sinensis Modulates Telomerase in Collagen-Induced Arthritis

Jalali

Saadat

2017

Zahedan J Res Med Sci

View full text Add to dashboard Cite

show abstract

“…Contrarily, it has been shown that EGCG inhibits the PI3K/Akt system in fibroblast cells (12) and the phosphorylation of ERK and Akt kinases in epidermal growth factor (EGF)-stimulated cells (13). More recently, accumulating evidence indicates that EGCG can inhibit PI3K/Akt and MAPK signaling systems (14)(15)(16)(17).…”

Section: Abstract Background/aim: (-)-Epigallocatechin-3-gallate (Egmentioning

confidence: 99%

“…Effect of rapamycin on P-gp expression in HepG2 cells exposed to DOX. Recently, it has been indicated that EGCG has an inhibitory property against mTOR, as well as PI3K (17). Therefore, we investigated the effect of rapamycin on P-gp level as this agent inactivates mammalian target of ANTICANCER RESEARCH 37: 6071-6077 (2017) 6074 Figure …”

Section: Effects Of Egcg and Dox On The Phosphorylation Of Akt Erk1/mentioning

confidence: 99%

(–)-Epigallocatechin-3-gallate Down-regulates Doxorubicin-induced Overexpression of P-glycoprotein Τhrough the Coordinate Inhibition of PI3K/Akt and MEK/ERK Signaling Pathways

Satonaka

Ishida

Takai

et al. 2017

View full text Add to dashboard Cite

Abstract. Background/Aim: (-)-Epigallocatechin-3-gallate (EGCG) has been indicated to regulate the function of Pglycoprotein (P-gp), which is a drug transporter encoded by the MDR1 (ABCB1) gene. P-gp expression is induced by doxorubicin (DOX). We aimed to clarify the mechanisms and inhibitory effects of EGCG on DOX-induced P-gp expression in HepG2 cells. Materials and Methods: Rhodamine 123 (Rho123) was used for P-gp substrate. Western blotting and polymerase chain reactions (PCRs) were conducted using specific antibodies and primer sets. Results: The DOXpretreated cells accumulated a significantly decreased amount of Rho123), than control cells; however, the cells pretreated with EGCG and DOX, in combination, accumulated Rho123 more than DOX-pretreated cells. DOX induced the overexpression of MDR1 mRNA and increased the phosphorylation of Akt, ERK1/2, p38 MAPK and JNK. EGCG significantly inhibited the phosphorylation of Akt and ERK. The DOX-induced P-gp overexpression was partially suppressed by an inhibitor of MEK1/2 (U0126), but not by a PI3K inhibitor (LY294002). Interestingly, the expression of P-gp was synergistically inhibited by combined treatment of U0126 with LY294002 and also inhibited by an mTORC1 inhibitor, rapamycin. Conclusion: EGCG inhibited DOX-induced overexpression of P-gp through the coordinate inhibitory action on MEK/ERK and PI3K/Akt signaling pathways.(-)-Epigallocatechin gallate (EGCG) is the most abundant component of tea polyphenols having various profitable properties, including anti-oxidative activity and cancerpreventive effect (1). In addition, concerning antitumor drug resistance, EGCG has been shown to decrease doxorubicin (DOX) resistance in a human carcinoma xenograft model mice (2) and inhibit the transport function of P-glycoprotein (P-gp), an export drug transporter causing antitumor multidrug resistance (MDR) in tumor cells (3)(4)(5).Human P-gp is a plasma membrane protein of 170 kDa encoded by the MDR1 (ABCB1) gene. The expression of MDR1 gene and P-gp is affected by various chemical substances and physico-chemical stress (5-7). We have previously suggested that the P-gp level was up-regulated through the activation of protein kinase C/nuclear factor-ĸB (PKC/NF-ĸB) in rats with streptozotocin-induced diabetes (8). Further, the expression of MDR1 gene has been also shown to be induced by PI3K/Akt/NF-ĸB signaling (9,10).EGCG has been shown to activate ERK and PI3K/Akt signaling and induce antioxidant enzymes in human mammary epithelial cells (11). Contrarily, it has been shown that EGCG inhibits the PI3K/Akt system in fibroblast cells (12) and the phosphorylation of ERK and Akt kinases in epidermal growth factor (EGF)-stimulated cells (13). More recently, accumulating evidence indicates that EGCG can inhibit PI3K/Akt and MAPK signaling systems (14)(15)(16)(17).From these backgrounds, in the present study, we aimed to clarify whether EGCG could suppress MDR and inhibit the induction of P-gp overexpression by DOX through inhibition of PI3K/Akt and ERK/MAPK signal transduction s...

show abstract

“…Both in vitro and in vivo experiments have revealed that green tea and EGCG could prevent steatosis by reducing dietary absorption of lipids and carbohydrates, and by the inhibition of adipose tissue breakdown, and de novo lipogenesis in both hepatic and adipose tissues, through the stimulation of β-oxidation and thermogenesis in the liver, and by improving insulin sensitivity. Furthermore, EGCG may inhibit the development of steatohepatitis from fatty liver disease, through its antioxidant and antiinflammatory characteristics [47] . Currently, there are no randomized, controlled trials in humans, evaluating the effects of green tea on NAFLD.…”

Section: Green Tea Extractmentioning

confidence: 99%