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高剂量绿茶多酚通过下调抗氧化酶和热休克蛋白表达诱导葡聚糖硫酸钠诱导结肠炎小鼠的肾毒性。

High-dose green tea polyphenols induce nephrotoxicity in dextran sulfate sodium-induced colitis mice by down-regulation of antioxidant enzymes and heat-shock protein expressions.

机构信息

Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Japan.

出版信息

Cell Stress Chaperones. 2011 Nov;16(6):653-62. doi: 10.1007/s12192-011-0280-8. Epub 2011 Jul 16.

Abstract

Previously, we reported that oral feeding of 1% green tea polyphenols (GTPs) aggravated the dextran sulfate sodium (DSS)-induced colitis in mice. In the present study, we assessed the toxicity of 1% GTPs in several organs from normal and DSS-exposed mice. Sixty-two male ICR mice were initially divided into four groups. Non-treated group (group 1, n = 15) was given standard diet and water, GTPs (group 2, n = 15) received 1% GTPs in diet and water, DSS (group 3, n = 15) received diet and 5% DSS in water, and GTPs + DSS group (group 4, n = 17) received 1% GTPs in diet and 5% DSS in water. We found that group 4 significantly increased (P < 0.05) kidney weight, the levels of serum creatinine and thiobarbituric acid-reactive substances in both kidney and liver, as compared with those in group 3. The mRNA expression levels of antioxidant enzymes and heat-shock proteins (HSPs) in group 4 were lower than those of group 3. For instance, heme oxygenase-1 (HO-1), HSP27, and 90 mRNA in the kidney of group 4 were dramatically down-regulated as compared with those of group 3. Furthermore, 1% GTPs diet decreased the expression of HO-1, NAD(P)H:quinone oxidoreductase 1 (NQO1) and HSP90 in kidney and liver of non-treated mice. Taken together, our results indicate that high-dose GTPs diet disrupts kidney functions through the reduction of antioxidant enzymes and heat-shock protein expressions in not only colitis but also non-treated ICR mice.

摘要

先前,我们报道了口服 1%绿茶多酚(GTPs)会加重葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎。在本研究中,我们评估了 1%GTPs 在正常和 DSS 暴露的小鼠几种器官中的毒性。62 只雄性 ICR 小鼠最初分为四组。未处理组(第 1 组,n=15)给予标准饮食和水,GTPs 组(第 2 组,n=15)给予饮食和水中的 1%GTPs,DSS 组(第 3 组,n=15)给予饮食和水中的 5%DSS,GTPs+DSS 组(第 4 组,n=17)给予饮食和水中的 1%GTPs 和 5%DSS。我们发现与第 3 组相比,第 4 组的肾脏重量、血清肌酐和肝肾中硫代巴比妥酸反应物质的水平显著增加(P<0.05)。第 4 组的抗氧化酶和热休克蛋白(HSPs)的 mRNA 表达水平低于第 3 组。例如,第 4 组肾脏中的血红素加氧酶-1(HO-1)、HSP27 和 90mRNA 的表达水平与第 3 组相比显著下调。此外,1%GTPs 饮食降低了非处理小鼠肾脏和肝脏中 HO-1、NAD(P)H:醌氧化还原酶 1(NQO1)和 HSP90 的表达。综上所述,我们的结果表明,高剂量 GTPs 饮食通过降低抗氧化酶和热休克蛋白的表达,不仅破坏了结肠炎小鼠的肾脏功能,也破坏了非处理 ICR 小鼠的肾脏功能。

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