Enhancing Effect of Zinc on Hepatoprotectivity of Epigallocatechin Gallate in Isolated Rat Hepatocytes.

Kagaya, Noritaka; Kawase, Masaya; Maeda, Hatsuo; Tagawa, Yoh‐ichi; Nagashima, Hitoshi; Ohmori, Hidenobu; Yagi, Kiyohito

doi:10.1248/bpb.25.1156

Cited by 26 publications

(18 citation statements)

References 24 publications

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“…However, in the present report (Fig. 2) and a previous report [14], the induction of MT did not appear to protect against hepatotoxicity, since zinc itself is unable to protect cells against bromobenzene-induced damage. This is supported by the study of occur in the present in vitro study.…”

Section: Discussioncontrasting

confidence: 90%

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Liver Protection by Bis(Maltolato)Zinc(II) Complex

et al. 2004

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Abstract:The aim of this study was to perform screening of a novel drug for treating liver injury. Bis(maltolato)zinc(II) complex [Zn(Mal) 2 ], which was previously reported to possess insulinomimetic activity, was found to have potency against experimentally induced liver injury both in vitro and in vivo. Cultured rat hepatocytes were treated with bromobenzene for 24 h to induce cellular injury. Zn(Mal) 2 of various concentrations was added along with bromobenzene in order to evaluate the hepatoprotective activity of Zn(Mal) 2 in vitro. The number of viable hepatocytes decreased by 42% in the culture with bromobenzene. However, hepatocyte viability was maintained when Zn(Mal) 2 was added to the bromobenzene culture. The hepatoprotective activity of Zn(Mal) 2 in vivo was investigated using a concanavalin A-induced liver injury model in BALB/c mice. Changes in serum aminotransferase activities and the secretion of several cytokines were measured. The hepatoprotective effect of Zn(Mal) 2 was also demonstrated in vivo by the suppression of serum aspartate aminotransferase and alanine aminotransferase elevation. No significant changes in serum cytokines associated with the induction of hepatic damage were observed in the concanavalin A-induced injury model. However, examination of concanavalin A-treated mouse splenocytes revealed a dose-dependent suppression of cytokine secretions by Zn(Mal) 2 . Zn(Mal) 2 possessed hepatoprotective activity and might exert its effect by a number of mechanisms.

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Section: Discussioncontrasting

confidence: 90%

“…We previously reported a catechin, epigallocatechin-3-gallate (EGCG), is an effective liverprotecting agent and the complex formation of EGCG with zinc enhances the potency of EGCG against cytotoxin-induced hepatotoxicity [14]. Based on this result, the zinc complex was considered to play a protective role in hepatotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Liver Protection by Bis(Maltolato)Zinc(II) Complex

et al. 2004

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“…Accordingly, catechin could form 1:1 complex with either Zn 2+ or Cu 2+ , which can be monitored through the linearization algorithms as competitive with pre-concentration of the metal ions on the mercury electrode (Esparza et al, 2005). Kagaya et al(2002) reported that it was the formation of zinc-EGCG complex that enhanced effect of zinc on hepatoprotectivity of EGCG in isolated rat hepatocytes. These observations give a hint that the biological behavior of EGCG was changed in the presence of extracellular zinc, due maybe to the formation of zinc-EGCG complex.…”

Section: +mentioning

confidence: 99%

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

Yang

Sun

et al. 2009

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To evaluate effects of epigallocatechin-3-gallate (EGCG) on the viability, membrane properties, and zinc distribution, with and without the presence of Zn . The proportion of EGCG incorporated into liposomes treated with the mixture of EGCG and Zn 2+ 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 Zn 2+. 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 Zn 2+ could attenuate the actions elicited by EGCG.

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“…Thus, various desirable effects of flavonoids, such as anticancer and antioxidant activities, are found to be enhanced by metal ions. Zinc ions were also found to enhance the hepatoprotective effect of catechins (Kagaya et al, 2002). This result suggests that the metals and catechins interact, and this contributes to the effect in vitro.…”

Section: Introductionmentioning

confidence: 73%