Immunoregulatory Effect and Mechanism of Epigallocatechin-3-Gallate in A Mouse Oral Cancer Model

Objective:This investigation delineates the anti-cancer potency of epigallocatechin-3-gallate(EGCG)in an oral cancer mouse model,with a focus on its effect on T-cell activation.Methods:An oral cancer model was established in male Balb/c mice using 4-nitroquinoline 1-oxide(4-NQO).The mice were systematically grouped and administered graded concentrations of EGCG.Key parameters such as body weight,hydration levels,tumor volume,and mass were meticulously tracked.T-cell activity and cytokine expression profiles,focusing on interleukin-2(IL-2),interferon-gamma(IFN-γ),and tumor necrosis factor-alpha(TNF-α),were quantified using ELISA.A comprehensive statistical evaluation included one-way ANOVA,Tukey’s HSD multiple comparison test,and the Kruskal-Wallis non-parametric assessment.Results:EGCG-administered cohorts exhibited a pronounced reduction in tumor size and mass,with the high-dose group showing the greatest efficacy.ELISA findings corroborated a significant increase in T-cell activity and concomitant upregulation of key cytokines,including IL-2,IFN-γ,and TNF-α(P<0.05).Conclusion:This investigation confirms the tumor-suppressive efficacy of EGCG in a murine oral squamous cell carcinoma model.The therapeutic effects of EGCG are mediated through T-cell activation and the upregulation of pivotal cytokine expression,highlighting its potential immunomodulatory role in oral cancer treatment.

Epigallocatechin-3-gallate treatment to promote neuroprotection and functional recovery after nervous system injury

Traumatic spinal cord injury （SCI） causes motor paralysis, sensory anesthesia and autonomic dysfunction below the le- sion site and additionally some SCI patients refer neuropathic pain together with these signs and symptoms. Clinical and experimental studies have revealed the main pathological changes of injured spinal cord implicated in all these signs and symptoms, including neuropathic pain. After few hours of traumatic SCI, it is usual to observe broken blood brain barrier with plasma and blood cells extravasation, cell necrosis, disruption of ascending and descending spinal cord pathways and increased potassium and glutamate. Glutamate contributes to excitotoxicity of neurons whereas potassium facilitates ectopic depolarization of survival neurons and activation of resident microglia.

Study on Preparation Process of Effervescent Tablets Made from EGCG of Tea

[ Objectivel The study aimed to discuss the preparation process of Epigallocatechin-3-gallate （EGCG） effervescent tablets. [ Method] Various raw materials were dried for different time at 50℃, and then the sticking degree of EGCG effervescent tablets was reviewed. Hereafter, the formula of EGCG effervescent tablets was optimized by orthogonal test. [ Result] Effervescent tablets without sticking were smooth after being dried for 150 rain. The optimal formula of EGCG effervescent tablets was composed of 4% EGCG, 45% citric acid and sodium carbonate （Citric acid： Sodium carbonate = 1.6：1 ）, 20% lactose, 4% L-leucine, 4% sodium cyclamate and 23% orange powder. [Condusion] The prepared EGCG effervescent tablets without sticking has a good effervescence effect and taste.

Epigallocatechin-3-gallate affects the growth of LNCaP cells via membrane fluidity and distribution of cellular zinc

Objective:To evaluate effects of epigallocatechin-3-gallate (EGCG) on the viability, membrane properties, and zinc distribution, with and without the presence of Zn2+, in human prostate carcinoma LNCaP cells. Methods: We examined changes in cellular morphology and membrane fluidity of LNCaP cells, distribution of cellular zinc, and the incorporated portion of EGCG after treatments with EGCG, Zn2+, and EGCG+Zn2+. Results: We observed an alteration in cellular morphology and a decrease in membrane fluidity of LNCaP cells after treatment with EGCG or Zn2+. The proportion of EGCG incorporated into liposomes treated with the mixture of EGCG and Zn2+ at the ratio of 1:1 was 90.57%, which was significantly higher than that treated with EGCG alone (30.33%). Electron spin resonance (ESR) studies and determination of fatty acids showed that the effects of EGCG on the membrane fluidity of LNCaP were decreased by Zn2+. EGCG accelerated the accumulation of zinc in the mitochondria and cytosol as observed by atomic absorption spectrometer. Conclusion: These results show that EGCG interacted with cell membrane, decreased the membrane fluidity of LNCaP cells, and accelerated zinc accumulation in the mitochondria and cytosol, which could be the mechanism by which EGCG inhibits proliferation of LNCaP cells. In addition, high concentrations of Zn2+ could attenuate the actions elicited by EGCG.

Potential effect of EGCG on the anti-tumor efficacy of metformin in melanoma cells

Metformin,a first-line drug for type 2 diabetes mellitus,has been recognized as a potential anti-tumor agent in recent years.Epigallocatechin-3-gallate(EGCG),as the dominant catechin in green tea,is another promising adjuvant agent for tumor prevention.In the present work,the potential effect of EGCG on the anti-tumor efficacy of metformin in a mouse melanoma cell line(B16F10)was investigated.Results indicated that EGCG and metformin exhibited a synergistic effect on cell viability,migration,and proliferation,as well as signal transducer and activator of transcription 3/nuclear factor-κB(STAT3/NF-κB)pathway signaling and the production of inflammation cytokines.Meanwhile,the combination showed an antagonistic effect on cell apoptosis and oxidative stress levels.The combination of EGCG and metformin also differentially affected the nucleus(synergism)and cytoplasm(antagonism)of B16F10 cells.Our findings provide new insight into the potential effects of EGCG on the anti-tumor efficacy of metformin in melanoma cells.

Cloning of a caffeoyl-coenzyme A O-methyltransferase from Camellia sinensis and analysis of its catalytic activity

Epigallocatechin-3-O-（3-O-methyl） gallate（EGCG3＂Me） present in leaves of Camellia sinensis has many beneficial biological activities for human health. However, EGCG3＂Me occurs naturally in tea leaves in extremely limited quantities. Finding an enzyme from C. sinensis to catalyze the synthesis of EGCG3＂Me is an alternative method to make up for the scarcity of EGCG3＂Me in natural situations. In the present study, a complementary DNA（c DNA） encoding region and genomic DNA of the caffeoyl-coenzyme A O-methyltransferase（CCo AOMT） gene were isolated from C. sinensis（designated Cs CCo AOMT）. Nucleotide sequence analysis of Cs CCo AOMT revealed an open reading frame of 738 bp that encodes a polypeptide with a predicted molecular weight of 28 k Da, which correlated well with the results of sodium dodecyl sulfate-polyacrylamide gel electrophoresis（SDS-PAGE）. The full-length DNA sequence（2678 bp） contained five exons and four introns. The deduced amino acid sequence of Cs CCo AOMT shared 92% identity with CCo AOMTs from Codonopsis lanceolata and Betula luminifera. The catalytic activity of Cs CCo AOMT was analyzed. Three monomethylated epigallocatechin-3-O-gallate（EGCG） compounds（EGCG4＂Me, EGCG3＂Me, and EGCG3＇Me） were produced by Cs CCo AOMT with K m in the micromolar range. Real-time polymerase chain reaction（RT-PCR） experiments indicated that the Cs CCo AOMT transcript was present at low levels during the early stages of leaf maturity（the first leaf and bud on a shoot） but the relative expression was augmented at advanced stages of leaf maturity（the third or fourth leaf on a shoot）, which accorded well with changes in EGCG3＂Me content in fresh leaves. Hence, we concluded that Cs CCo AOMT catalyzes the syntheses of methylated EGCGs.