Anti-apoptotic activity of caffeic acid, ellagic acid and ferulic acid in normal human peripheral blood mononuclear cells: A Bcl-2 independent mechanism

Khanduja, Krishan Lal; Avti, Pramod K.; Kumar, Subodh; Mittal, Nidhi; Sohi, Kiranjit Kaur; Pathak, Chander Mohan

doi:10.1016/j.bbagen.2005.12.017

Cited by 121 publications

(82 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…EA has been found to possess various pharmacological properties as anticarcinogenic, antioxidant, antifibrosis, and chemopreventive properties [9][10][11] . Numerous scientific reports have evaluated the anticancer property of EA both in vivo and in vitro models for various kinds of cancer such as thyroid, breast, prostate, urinary bladder and blood cancer [12][13][14][15] . In spite of these findings, the inhibition of glioblastoma growth by EA has been rarely reported.…”

Section: Introductionmentioning

confidence: 99%

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

et al. 2016

View full text Add to dashboard Cite

PURPOSE:To investigate the anticancer activity of ellagic acid (EA) in U251 human glioblastoma cells and its possible molecular mechanism. METHODS:The cells were treated with EA at various concentrations for different time periods. Cell viability and cell proliferation were detected by cell counting kit-8(CCK-8) assay and live/dead assay respectively. Cell apoptosis were measured with Annexin V-FITC/PI double staining method by flow cytometry and Mitochondrial membrane potential assay separately. Cell cycle was measured with PI staining method by flow cytometry. The expressions of Bcl-2, Survivin, XIAP, Caspase-3, Bax, JNK, p-JNK, ERK1/2, p-ERK1/2, p38, p-p38, DR4, DR5, CHOP and GRP78-related proteins were detected by western blot after EA treatment. RESULTS:Cell viability and proliferation of glioblastoma cells treated with EA were significantly lower than the control group. EA caused robust apoptosis of the glioblastoma cells compared to the control group. EA significantly decreased the proportion at G0/ G1 phases of cell cycling accompanied by increased populations at S phase in U251 cell lines. And the expressions of anti-apoptotic proteins were dramatically down-regulated. CONCLUSION:Ellagic acid potentially up-regulated DR4, DR5 and MAP kinases (JNK, ERK1/2 and p38). EA also caused significant increase in the expressions of CHOP and GRP78. Our findings suggest that EA would be beneficial for the treatment of glioblastoma.

show abstract

Section: Introductionmentioning

confidence: 99%

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Meanwhile, FA exhibited antioxidant activity at significantly lower concentrations in cell cultures (1-200 µm). [18][19][20] Thus, the inhibition of mTor by FA appeared in a role that was distinct from that of its antioxidant activity. Autophagy significantly contributes to cellular quality control by removing unfolded and denatured proteins.…”

Section: Resultsmentioning

confidence: 99%

“…As is the case with other polyphenols, FA significantly reduces lipid peroxidation and protein oxidation. 2,3) Stimulation of phosphatidylinositol 3-kinase (PI3-kinase) and extracellular signal-regulated kinase by FA has been proposed as an underlying mechanism, which eventually causes nuclear factor erythroid 2-related factor 2 nuclear translocation. Through this effect, FA enhances the expression of anti-oxidant enzymes and elevates reduced glutathione levels.…”

mentioning

confidence: 99%

Ferulic Acid Induces Mammalian Target of Rapamycin Inactivation in Cultured Mammalian Cells

Bian

Furuya

Zheng

et al. 2013

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Ferulic acid (FA), a naturally occurring polyphenol abundant in vegetables and rice bran, is known to possess a potent antioxidant activity, thereby protecting cells from oxidative stress. In the present study, we show that in addition to its known anti-oxidant activity, ferulic acid exerts substantial inhibitory activity on cellular mammalian target of rapamycin (mTor)-signaling pathways. In HeLa cells and mouse primary hepatocytes cultured with conventional nutrient-rich media, ferulic acid (1 mm) elicited dephosphorylation of S6 kinase and its substrate ribosomal S6. The dephosphorylating activity of ferulic acid was almost comparable to that of rapamycin, an established mTor inhibitor (TORC1). We next investigated the effect of ferulic acid on autophagy, a major cellular degradative process, which significantly contributes to the maintenance of cell homeostasis. Using a conventional green fluorescent protein-microtubule-associated protein IA/IB light chain 3 (GFP-LC3) dot assay to evaluate autophagy flux, we showed that ferulic acid caused a significant increase in GFP-LC3 dots under serum-rich conditions in HeLa cells. The enhancement of autophagic flux by ferulic acid was almost equivalent to that of rapamycin. Furthermore, ferulic acid significantly enhanced autophagic degradation of 14 C-leucine-labeled long-lived proteins of cultured mouse hepatocytes under nutrient-rich conditions, but not nutrient-deprived conditions. These results indicate that ferulic acid is almost the equivalent of rapamycin in the ability to inhibit mTor (TORC1), which makes it a potent activator of basal autophagy.Key words ferulic acid; ribosomal S6; S6 kinase; mammalian target of rapamycin; autophagy; microtubuleassociated protein IA/IB light chain 3Ferulic acid [(E)-3-(4-hydroxy-3-methoxy-phenyl) prop-2-enoic acid] (FA) is a polyphenolic compound abundant in vegetables, and in particular, artichokes, eggplant, and rice bran. 1) Because polyphenols are known to possess potent antioxidant activity, they have been widely used for the prevention of reactive oxygen species (ROS)-related diseases such as cancer, neurodegenerative and inflammatory diseases. As is the case with other polyphenols, FA significantly reduces lipid peroxidation and protein oxidation.2,3) Stimulation of phosphatidylinositol 3-kinase (PI3-kinase) and extracellular signal-regulated kinase by FA has been proposed as an underlying mechanism, which eventually causes nuclear factor erythroid 2-related factor 2 nuclear translocation. Through this effect, FA enhances the expression of anti-oxidant enzymes and elevates reduced glutathione levels. 4)Recently, the neuroprotective effect of FA has attracted more attention. Oral pre-administration of FA (ca. 17 mg/ kg per day for 4 weeks) has ameliorated memory deficits in mice caused by intracerebroventicular injection of amyloid beta (Aβ 42 ).5) Effective suppression of interleukin (IL)-β expression in the hippocampus by FA is thought to exert an anti-inflammatory effect on learning and memory deficits of Aβ 42 -admi...

show abstract

“…The data obtained in vivo support the ability of kaempferol and ferulic acid to counteract cytokine-induced β-cells injury [43,44] . Antiapoptotic properties of hydroxicinnamic acids, which are one of the most important GW components, are also principally possible (confirmed in peripheral blood mononuclear cells [45] ).…”

Section: Figure5 Photomicrographs Of the Liver Of The Alloxan-inducementioning

confidence: 99%

The Efficacy of Goutweed (Aegopodium Podagraria L.) Tincture and Metformin Combination in the Early Stages of AlloxanInduced Diabetes in Rats

2017

ARC Journal of Diabetes and Endocrinology

View full text Add to dashboard Cite

Anti-apoptotic activity of caffeic acid, ellagic acid and ferulic acid in normal human peripheral blood mononuclear cells: A Bcl-2 independent mechanism

Cited by 121 publications

References 41 publications

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

Ferulic Acid Induces Mammalian Target of Rapamycin Inactivation in Cultured Mammalian Cells

The Efficacy of Goutweed (Aegopodium Podagraria L.) Tincture and Metformin Combination in the Early Stages of AlloxanInduced Diabetes in Rats

Contact Info

Product

Resources

About