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没食子儿茶素没食子酸酯对 Wistar 大鼠二甲基肼诱导的结肠毒性的改善作用。

Amelioration of N,N'-dimethylhydrazine induced colon toxicity by epigallocatechin gallate in Wistar rats.

机构信息

Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology and Toxicology, School of Chemical and Life Sciences, 28848Jamia Hamdard, New Delhi, India.

Department of Pharmacology and Toxicology, College of Pharmacy, 204568Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia.

出版信息

Hum Exp Toxicol. 2021 Sep;40(9):1558-1571. doi: 10.1177/09603271211002884. Epub 2021 Mar 23.

DOI:10.1177/09603271211002884
PMID:33754881
Abstract

Colon cancer is a life-threatening disease all over the world and is linked to constant oxidative stress and inflammation. Epigallocatechin gallate (EGCG), is a naturally occurring flavone possessing health benefiting pharmacological properties including antioxidant, anti-inflammatory and free radical scavenging properties. Our study investigates the role of EGCG on N,N'-dimethylhydrazine (DMH), a toxic environmental pollutant, induced colon toxicity. To investigate the effect of EGCG, Wistar rats were given EGCG for 7 days at the two doses of 10 and 20 mg/kg body weight and DMH was injected on the seventh day in all the group rats except the control. Our results indicate that DMH administration increased the oxidative stress (MDA) and depleted the glutathione and antioxidant enzyme activities (SOD, CAT, GR, GST and GPx) which was significantly ameliorated by EGCG treatment. Additionally DMH treatment upregulated inflammatory markers expression (NF-κB, COX-2 and IL-6) and enhanced mucosal damage in the colon. EGCG treatment significantly reduced inflammation and restored the normal histoarchitecture of the colon. We can conclude from the present study findings that EGCG protects the colon from DMH toxicity through its antioxidant and anti-inflammatory potential.

摘要

结肠癌是一种在全球范围内危及生命的疾病,与持续的氧化应激和炎症有关。表没食子儿茶素没食子酸酯(EGCG)是一种天然存在的类黄酮,具有抗氧化、抗炎和清除自由基等有益的药理特性。我们的研究调查了 EGCG 对 N,N'-二甲基肼(DMH)的作用,DMH 是一种有毒的环境污染物,可诱导结肠毒性。为了研究 EGCG 的作用,我们给 Wistar 大鼠连续 7 天分别给予 10 和 20mg/kg 体重的 EGCG,除对照组外,所有组的大鼠在第 7 天都注射 DMH。我们的结果表明,DMH 给药增加了氧化应激(MDA),耗尽了谷胱甘肽和抗氧化酶活性(SOD、CAT、GR、GST 和 GPx),而 EGCG 治疗显著改善了这种情况。此外,DMH 处理上调了炎症标志物的表达(NF-κB、COX-2 和 IL-6),并增强了结肠的粘膜损伤。EGCG 治疗显著减轻了炎症并恢复了结肠的正常组织形态。从本研究的结果可以得出结论,EGCG 通过其抗氧化和抗炎潜力保护结肠免受 DMH 毒性的侵害。

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