Protective effects of ellagic acid on ethanol-induced toxicity in hepatic HepG2 cells

Sohn, Eun‐Hwa; Koo, Hyun Jung; Hang, Đo Thi Thu; Jang, Seon‐A; Namkoong, Seung; Lim, Jung Dae; Kang, Se Chan

doi:10.1007/s13273-013-0032-1

Cited by 19 publications

(16 citation statements)

References 42 publications

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“…The inhibitory effect of EA or Sennoside B on proliferation was attributed to the induction of cell cycle arrest. The data regarding the effects of EA on osteosarcoma are consistent with previous studies in other cancer types ( 7 – 11 ). However, the inhibitory effects of Sennoside B were demonstrated for the first time, to the best of our knowledge.…”

Section: Discussionsupporting

confidence: 90%

“…Ellagic acid (EA) is a polyphenol compound with strong antioxidant properties that is found as ellagitannins in the fruits and nuts of several plants. The oral administration of EA can protect the system from alcohol toxicity by decreasing the expression of liver marker enzymes and increasing the activity of the antioxidant cascade ( 6 , 7 ); it was previously demonstrated to induce apoptosis and cell cycle arrest in various types of cancer cell ( 8 – 11 ). However, its potential anti-tumor role in osteosarcoma and the mechanisms for its effects remain elusive.…”

Section: Introductionmentioning

confidence: 99%

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Ellagic acid and Sennoside B inhibit osteosarcoma cell migration, invasion and growth by repressing the expression of c‑Jun

Wang

et al. 2018

Oncol Lett

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Osteosarcoma is a mesenchymally derived, high-grade bone sarcoma that is the most frequently diagnosed primary malignant bone tumor. Today, chemoprevention is regarded as a promising and realistic approach in the prevention of human cancer. Previous studies have suggested ellagic acid (EA) and Sennoside B have potential in this regard. The aim of the present study was to elucidate the anti-osteosarcoma effects of EA and Sennoside B by using Saos-2 and MG63 osteosarcoma cells. It was identified that EA or Sennoside B treatment could inhibit the growth, migration and invasion of the cells, and induce G1 cell cycle arrest by repressing the transcription of c-Jun. These results may provide a cellular basis for the application of EA or Sennoside B in the treatment of patients with osteosarcoma.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Ellagic acid and Sennoside B inhibit osteosarcoma cell migration, invasion and growth by repressing the expression of c‑Jun

Wang

et al. 2018

Oncol Lett

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“…3 ), we further studied the mechanisms of the beneficial effects by its individual components UA and EA on oxidative stress and inflammation-related mRNAs upregulated after binge alcohol exposure. Based on the previous studies with UA [37] and EA [38] , AML12 normal liver cells were treated with 100 mM ethanol in the absence or presence of UA, EA, or CMZ for 24 h. Confocal microscopy image showed that binge alcohol significantly increased the CYP2E1 expression. However, pretreatment with UA or EA at the indicated concentration decreased the CYP2E1 expression in ethanol-exposed AML12 cells, as comparable to that treated with CMZ, a specific inhibitor of CYP2E1 transcription ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Pomegranate prevents binge alcohol-induced gut leakiness and hepatic inflammation by suppressing oxidative and nitrative stress

Cho

Song

2018

Redox Biology

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Alcoholic liver disease (ALD) is a major chronic liver disease worldwide and can range from simple steatosis, inflammation to fibrosis/cirrhosis possibly through leaky gut and systemic endotoxemia. We investigated whether pomegranate (POM) protects against binge alcohol-induced gut leakiness, endotoxemia, and inflammatory liver damage. After POM pretreatment for 10 days, rats were exposed to 3 oral doses of binge alcohol (5 g/kg/dose) or dextrose (as control) at 12-h intervals. Binge alcohol exposure induced leaky gut with significantly elevated plasma endotoxin and inflammatory fatty liver by increasing the levels of oxidative and nitrative stress marker proteins such as ethanol-inducible CYP2E1, inducible nitric oxide synthase, and nitrated proteins in the small intestine and liver. POM pretreatment significantly reduced the alcohol-induced gut barrier dysfunction, plasma endotoxin and inflammatory liver disease by inhibiting the elevated oxidative and nitrative stress marker proteins. POM pretreatment significantly restored the levels of intestinal tight junction (TJ) proteins such as ZO-1, occludin, claudin-1, and claundin-3 markedly diminished after alcohol-exposure. In addition, the levels of gut adherent junction (AJ) proteins (e.g., β-catenin and E-cadherin) and desmosome plakoglobin along with associated protein α-tubulin were clearly decreased in binge alcohol-exposed rats but restored to basal levels in POM-pretreated rats. Immunoprecipitation followed by immunoblot analyses revealed that intestinal claudin-1 protein was nitrated and ubiquitinated in alcohol-exposed rats, whereas these modifications were significantly blocked by POM pretreatment. These results showed for the first time that POM can prevent alcohol-induced gut leakiness and inflammatory liver injury by suppressing oxidative and nitrative stress.

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“…It has been well established that ellagic acid exhibits anticancer (19), antimutagen (20–22) and antimicrobial functions (23), as well as others. Numerous studies concerning the antimutagen and anticancer effects of ellagic acid were performed in the 1970s (24–27).…”

Section: Discussionmentioning

confidence: 99%

Antitumor effect and mechanism of an ellagic acid derivative on the HepG2 human hepatocellular carcinoma cell line

Zhang

Guo

et al. 2013

Oncology Letters

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In the present study, to identify the effective components of Chinese traditional herbs, Euphorbia hylonoma Hand.-Mazz. (Euphorbiaceae), a folk herb that has been used among the Qinling mountain area for hundreds of years, was investigated. 3,3′-Di-O-methyl ellagic acid-4′-O-β-d-xylopyranoside (JNE2), an ellagic acid derivative, was isolated from the acetone extract of the herb and its antitumor activity against human hepatoma HepG2 cells was detected in vitro. The results showed that JNE2 inhibited the proliferation of HepG2 cells in a dose- and time-dependent manner and blocked the cell cycle at the G1/S phase. A high dosage of JNE2 induced apoptosis of the tumor cells, but no significant differences were identified between the treatment groups. The invasiveness of HepG2 cells was also inhibited by JNE2. The mechanism of the antitumor effect of JNE2 at the molecular level was presumed to be due to the upregulation of the protein expression of Bax and caspase-3, and the downregulation of the protein expression of Bcl-2 and CCND1. The results suggested that JNE2 is a potential antitumor agent that merits further investigation.

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Protective effects of ellagic acid on ethanol-induced toxicity in hepatic HepG2 cells

Cited by 19 publications

References 42 publications

Ellagic acid and Sennoside B inhibit osteosarcoma cell migration, invasion and growth by repressing the expression of c‑Jun

Ellagic acid and Sennoside B inhibit osteosarcoma cell migration, invasion and growth by repressing the expression of c‑Jun

Pomegranate prevents binge alcohol-induced gut leakiness and hepatic inflammation by suppressing oxidative and nitrative stress

Antitumor effect and mechanism of an ellagic acid derivative on the HepG2 human hepatocellular carcinoma cell line

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