Cytoprotective effect of epigallocatechin-3-gallate against deoxynivalenol-induced toxicity through anti-oxidative and anti-inflammatory mechanisms in HT-29 cells

Kalaiselvi, Palaniswamy; Krishnaswamy, Rajashree; Priya, Lohanathan Bharathi; Padma, Viswanadha Vijaya

doi:10.1016/j.fct.2013.01.042

Cited by 75 publications

(64 citation statements)

References 39 publications

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“…8) In addition, EGCG was confirmed to directly inhibit protein kinases by working as an ATP analog. 9) Previously, we reported the therapeutic effect of EGCG in vitiligo induced by monobenzone in mice.…”

mentioning

confidence: 99%

Epigallocatechin-3-gallate (EGCG) Suppresses the Trafficking of Lymphocytes to Epidermal Melanocytes <i>via</i> Inhibition of JAK2: Its Implication for Vitiligo Treatment

Ning

Wang

Dong

et al. 2015

Biological & Pharmaceutical Bulletin

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Vitiligo is an inflammatory skin disorder in which activated T cells play an important role in its onset and progression. Epigallocatechin-3-gallate (EGCG), the major chemical constituent of green tea, exhibits remarkable anti-oxidative and anti-inflammatory properties. EGCG administration has been confirmed to decrease the risk of vitiligo; however, the underlying mechanism is undetermined. In this study, we proved that EGCG directly inhibited the kinase activity of Janus kinase 2 (JAK2). In primary cultured human melanocytes, EGCG pre-treatment attenuated interferon ( Key words vitiligo; epigallocatechin-3-gallate; melanocyte; Janus kinase 2; chemoattractant Vitiligo is a depigmentation disorder caused by the destruction of epidermal melanocytes.1) The exact pathophysiological mechanism of vitiligo remains elusive. However, several hypotheses, including autoimmune, oxidant-antioxidant, genetic susceptibility, neural and viral mechanisms, have been proposed to explain the selective destruction of melanocytes. Currently, clinical and bench findings suggest the major role of autoimmune factors in the progress of vitiligo. Inflammatory cells, mostly T lymphocytes, have been identified close to vitiligous skin lesion.2,3) Lesional CD8+ T cells specially induce melanocyte apoptosis in unaffected skin ex vivo, and the frequency of anti-melanocyte CD8+ T cells in both the blood and skin of vitiligo patients correlates with the severity of disease. 4,5) Moreover, immunosuppressive therapies targeting T-cell activation have been shown to be effective for vitiligo treatment.6,7) These evidences all support a direct role for T lymphocytes in melanocyte destruction in human vitiligo.Epigallocatechin-3-gallate (EGCG), a major catechin in green tea, is considered beneficial for human health, especially as an anti-oxidative agent.8) In addition, EGCG was confirmed to directly inhibit protein kinases by working as an ATP analog.9) Previously, we reported the therapeutic effect of EGCG in vitiligo induced by monobenzone in mice. 10) Our results suggested that it could contribute to the suppression of CD8+ T cell migration and the inflammatory cytokine expression. However, the mechanism regarding the EGCG regulation of immune responses in vitiligo is still unclear.The aim of study is to elucidate the inhibitory effects of EGCG on inflammatory signaling pathways and to identify the target of EGCG inhibition. RESULTS AND DISCUSSION EGCG Inhibited Janus Kinase (JAK)2 Activity in VitroThe JAKs are a family of four non-receptor tyrosine kinases including JAK1, JAK2 JAK3 and tyrosine kinase (TYK)2. Recruitment of stimuli to cell surface receptors activates JAKs which, in turn, phosphorylates and stimulates latent cytoplasmic signal transducer and activator of transcription (STAT) proteins to an active dimer, leading to nuclear translocation and DNA binding and subsequently modulating gene transcription.11) The JAK/STAT signal pathway controls a number of important biological responses, including immune functions, cellular growth, cell...

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mentioning

confidence: 99%

Epigallocatechin-3-gallate (EGCG) Suppresses the Trafficking of Lymphocytes to Epidermal Melanocytes <i>via</i> Inhibition of JAK2: Its Implication for Vitiligo Treatment

Ning

Wang

Dong

et al. 2015

Biological & Pharmaceutical Bulletin

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“…For instance, catechin has shown to inhibit the activity of COX-2, 5-LOX, phospholipase A2, NO production, NF-κB activation and pro-inflammatory cytokines such as TNF-α, and multiple interleukins that is IL-1,-2,-6,-8, and-12. [232021] These compounds are the primary biomarkers frequently isolated in patients experiencing long term arthritis. The main proinflammatory cytokines involved in the pathogenesis of arthritis are TNF-α and IL-1 β.…”

Section: Discussionmentioning

confidence: 99%

“…[1] The major flavan in Uncaria gambir , catechin and prenylated flavonoids and stilbenoids, from the root bark of Morus alba L possess activities suggestive of benefits in arthritis including: (i) Inhibition of the activity of cyclooxygenase-2 (COX-2), lipoxygenase (5-LOX), and pro-inflammatory cytokines TNF-α, IL-1,-2,-6,-8, and-12[23] by catechin, (ii) anti-inflammatory activities,[4] (iii) suppression effect of T-cell migration, (iv) inhibition of CX chemokine receptor (CXCR-4)-mediated chemotaxis and extracellular signal-regulated kinases (MEK/ERK) pathway,[5] (v) inhibition of nitric oxide (NO) production, inducible NO synthase expression, prostaglandin E2 (PGE2) production, and activation of NF-κB[6] and (vi) inhibition of pro-inflammatory mediators such as COX-2, IL-1 β, and IL-6,[78] by prenylated flavonoids and stilbenoids from M. alba root bark extract have been reported. Therefore, a composition comprised of these well-studied plant extracts at a specific ratio may provide a benefit in alleviating symptoms associated with arthritis.…”

Section: Introductionmentioning

confidence: 99%

Analgesic and anti-Inflammatory effect of UP3005, a botanical composition Containing two standardized extracts of Uncaria gambir and Morus alba

Yimam¹,

Lee²,

Kim³

et al. 2015

Phcog Res

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Background:Osteoarthritis (OA) is a chronic debilitating degenerative joint disease characterized by cartilage degradation and synovial inflammation exhibited by clinical symptoms such as joint swelling, synovitis, and inflammatory pain. Present day pain relief therapeutics heavily relies on the use of prescription and over the counter nonsteroidal anti-inflammatory drugs as the first line of defense where their long-term usage causes detrimental gastrointestinal and cardiovascular-related side-effects. As a result, the need for evidence based safer and efficacious alternatives from natural sources to overcome the most prominent and disabling symptoms of arthritis is a necessity.Materials and Methods:Describe the anti-inflammatory and analgesic effect of UP3005, a composition that contains a standardized blend of two extracts from the leaf of Uncaria gambir and the root bark of Morus alba in carrageenan-induced rat paw edema, abdominal constriction (writhing’s) and ear swelling assays in mouse with oral dose ranges of 100–400 mg/kg.Results:In vivo, statistically significant improvement in pain resistance, and suppression of paw edema and ear thickness in animals treated with UP3005 were observed compared with vehicle-treated diseased rats and mice. Ibuprofen was used a reference compound in all the studies. In vitro, enzymatic inhibition activities of UP3005 were determined with IC50 values of 12.4 μg/ml, 39.8 μg/ml and 13.6 μg/ml in cyclooxygenase-2 (COX-1), COX-2 and lipoxygenase (5-LOX) enzyme activity assay, respectively.Conclusions:These data suggest that UP3005, analgesic and anti-inflammatory agent of botanical origin with balanced dual COX-LOX inhibition activity, could potentially be used for symptom management of OA.

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“…Reactive oxygen species (ROS) were reported to be responsible for EGCG-induced apoptosis in mesothelioma (27) and EGCG-induced ROS production in endometrial carcinoma cells (28). However, ROS were not involved in EGCG-induced apoptosis in human laryngeal epidermoid carcinoma (Hep2) cells (14), although EGCG reduced deoxynivalenol-induced ROS in HT-29 cells (29). In the present study, ROS were found to contribute to EGCG-induced apoptosis in Eca-109 and Te-1 cells.…”

Section: Discussionmentioning

confidence: 99%

Molecular mechanism of epigallocatechin-3-gallate in human esophageal squamous cell carcinoma in vitro and in vivo

Liu

Hou

et al. 2014

Oncology Reports

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Abstract. Epigallocatechin-3-gallate (EGCG), the major polyphenol of green tea, has been shown to inhibit proliferation in various types of tumors. However, few studies concerning the role and mechanism of EGCG in esophageal squamous cell carcinoma are available. Therefore, the antitumor mechanism of EGCG needs to be investigated. The present study aimed to examine the antitumor effect of EGCG on the human esophageal squamous cell carcinoma cell lines, Eca-109 and Te-1, in vitro and in vivo. Cell viability was assessed using the MTT assay and tumor formation and growth in murine xenograft models with or without EGCG treatment. Cell cycle analysis and levels of reactive oxygen species (ROS) were detected using flow cytometry. Apoptosis was measured by Annexin/propidium iodide staining. Caspase-3 cleavage and vascular endothelial growth factor (VEGF) expression were detected using western blot analysis and immunohistochemistry in tumor cell lines and tumor xenografts, respectively. The results showed that EGCG inhibited proliferation in the Eca-109 and Te-1 cells in a time-and dose-dependent manner. Tumor cells were arrested in the G 1 phase and apoptosis was accompanied by ROS production and caspase-3 cleavage. In a mouse model, EGCG significantly inhibited the growth of Eca-109 tumors by increasing the expression of cleaved-caspase-3 and decreasing VEGF protein levels. Taken together, the results suggest that EGCG inhibits proliferation and induces apoptosis through ROS production, caspase-3 activation, and a decrease in VEGF expression in vitro and in vivo. Furthermore, EGCG may have future clinical applications for novel approaches to treat esophageal squamous cell carcinoma.

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Cytoprotective effect of epigallocatechin-3-gallate against deoxynivalenol-induced toxicity through anti-oxidative and anti-inflammatory mechanisms in HT-29 cells

Cited by 75 publications

References 39 publications

Epigallocatechin-3-gallate (EGCG) Suppresses the Trafficking of Lymphocytes to Epidermal Melanocytes <i>via</i> Inhibition of JAK2: Its Implication for Vitiligo Treatment

Epigallocatechin-3-gallate (EGCG) Suppresses the Trafficking of Lymphocytes to Epidermal Melanocytes <i>via</i> Inhibition of JAK2: Its Implication for Vitiligo Treatment

Analgesic and anti-Inflammatory effect of UP3005, a botanical composition Containing two standardized extracts of Uncaria gambir and Morus alba

Molecular mechanism of epigallocatechin-3-gallate in human esophageal squamous cell carcinoma in vitro and in vivo

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