Caffeic acid phenethyl ester inhibits liver fibrosis in rats

Li, Mei

doi:10.3748/wjg.v21.i13.3893

Cited by 53 publications

(32 citation statements)

References 38 publications

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“…It was reported by others that Nrf2 protein levels are increased in dose-dependent manner of CAPE. [35][36][37] These hypotheses are confirmed by our data showing increased protein on Nrf2 in response to CS-induced oxidative stress in A549 cells.…”

Section: Discussionsupporting

confidence: 79%

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Küçükgül

2016

AJP

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Introduction: The main objective of this study was to evaluate the effect of antioxidative and antiapoptotic effects and underlying molecular mechanisms of caffeic acid phenethyl ester (CAPE) on human lung epithelial cells exposed to cigarette smoke (CS). Materials and Methods: Human alveolar epithelial A549 cells were exposed to CS and treated with various concentrations of CAPE for 24 h, and their effective concentrations were identified by cell viability assay (MTT). Antioxidant and anti-inflammatory effect of CAPE on nuclear erythroid related factor-2 (Nrf2) and nuclear factor-ĸβ (NF-ĸβ) protein levels were analyzed by Western blotting. Furthermore, caspase 8 gene expression level was analyzed by reverse transcription-quantitative polymerase chain reaction. Results: Low concentration CAPE pretreatment rescued 52% of CS-exposed A549 cells from death. CS upregulated gene expression level of caspase 8 by 4.28 fold. However, 2.5 µM CAPE pretreatment increased caspase 8 level by 52%. CS exposure also elevated NF-ĸβ (p65) protein level by 70%, however, CAPE pretreatment significantly reversed this activation. While CS exposure decreased Nrf2 protein levels by 48% as compared with the control group, CAPE pretreatment increased Nrf2 protein level two folds approximately according to CS group. Discussion: CAPE markedly decreased inflammatory transcription factor NF-kB and increased antioxidant response element Nrf2 protein expression levels in CS-exposed human alveolar cells. According to the data obtained from this study, CAPE could be used as a strategic alternative to support treatment of inflammatory and oxidative stress-induced lung diseases.

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Section: Discussionsupporting

confidence: 79%

Untitled

Küçükgül

2016

AJP

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“…It has been shown that caffeic acid phenethyl ester (CAPE), which is an active component of the propolis agent, has antioxidant, antimicrobic, immunomodulator, antifibrotic, and antiinflammatory properties [16][17][18]. It is structurally similar to flavonoids and involves two annular structures, one of which carries two hydroxyl groups.…”

Section: Introductionmentioning

confidence: 99%

Anti-Apoptotic and Anti-Oxidant Effects of Caffeic Acid Phenethyl Ester on Cadmium-Induced Testicular Toxicity in Rats

Erboğa

Kanter

Aktaş

et al. 2015

Biol Trace Elem Res

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Cadmium (Cd) is a serious environmental and occupational contaminant and may represent a serious health hazard to humans and other animals. Cd is reported to induce the generation of reactive oxygen species, and induces testicular damage in many species of animals. The goal of our study was to examine the anti-apoptotic and anti-oxidant effects of caffeic acid phenethyl ester (CAPE) on Cd-induced oxidative stress, apoptosis, and testicular injury in rats. A total of 40 male Wistar albino rats were divided into four groups: control, CAPE alone, Cd-treated, and Cd-treated with CAPE; each group consisted of 10 animals. To induce toxicity, Cd (1 mg/kg body weight) was dissolved in normal saline and subcutaneously injected into rats for 30 days. The rats in CAPE-treated group were given a daily dose of 10 μmol/kg body weight of CAPE by using intraperitoneal injection. This application was continued daily for a total of 30 days. To date, no examinations of the anti-apoptotic and anti-oxidant properties of CAPE on Cd-induced apoptosis, oxidative damage, and testicular injury in rat testes have been reported. CAPE-treated animals showed an improved histological appearance and serum testosterone levels in Cd-treated group. Our data indicate a significant reduction in the number of apoptotic cells in testis tissues of the Cd-treated group with CAPE treatment. Moreover, CAPE significantly suppressed lipid peroxidation, compensated deficits in the anti-oxidant defenses in testes tissue resulted from Cd administration. These findings suggest that the protective potential of CAPE in Cd toxicity might be due to its anti-oxidant and anti-apoptotic properties, which could be useful for achieving optimum effects in Cd-induced testicular injury.

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“…However, the mechanisms of up‐regulatory effect of Nrf2 by ICAB require further investigation. Similarly, caffeic acid, a natural polyphenolic compound which has been widely accepted as a hepatoprotective folk medicine, also exerts its hepatoprotective effects by inhibiting the oxidative stress via Nrf2 pathway …”

Section: Discussionmentioning

confidence: 99%

Protective effect of isochlorogenic acid B on liver fibrosis in non‐alcoholic steatohepatitis of mice

Liu

Huang

Niu

et al. 2018

Basic Clin Pharma Tox

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Liver fibrosis is a common symptom of non-alcoholic steatohepatitis (NASH) and a worldwide clinical issue. The miR-122/HIF-1α signalling pathway is believed to play an important role in the genesis of progressive fibrosis. Isochlorogenic acid B (ICAB), naturally isolated from Laggera alata, is verified to have antioxidative and hepatoprotective properties. The aim of this study was to investigate the effect of ICAB on liver fibrosis in NASH and its potential protective mechanisms. NASH was induced in a mouse model with a methionine- and choline-deficient (MCD) diet for 4 weeks, and ICAB was orally administered every day at three doses (5, 10 and 20 mg/kg). Pathological results indicated that ICAB significantly improved the pathological lesions of liver fibrosis. The levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and hepatic hydroxyproline (Hyp), cholesterol (CHO) and triglyceride (TG) were also significantly decreased by ICAB. In addition, ICAB inhibited hepatic stellate cells (HSCs) activation and the expressions of hepatic genes involved in liver fibrosis including LOX, TGF-β1, MCP-1, COL1α1 and TIMP-1. ICAB also attenuated liver oxidative stress through Nrf2 signalling pathway. What is more, the decreased levels of miR-122 and over-expression of hepatic HIF-1α could be reversed by ICAB treatment. These results simultaneously confirmed that ICAB had a significant protective effect on fibrosis in NASH by inhibiting oxidative stress via Nrf2 and suppressing multiple profibrogenic factors through miR-122/HIF-1α signalling pathway.

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Caffeic acid phenethyl ester inhibits liver fibrosis in rats

Abstract: The protective effects of CAPE against liver fibrosis may be due to its ability to suppress the activation of HSCs by inhibiting oxidative stress.

Cited by 53 publications

References 38 publications

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Anti-Apoptotic and Anti-Oxidant Effects of Caffeic Acid Phenethyl Ester on Cadmium-Induced Testicular Toxicity in Rats

Protective effect of isochlorogenic acid B on liver fibrosis in non‐alcoholic steatohepatitis of mice

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