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表没食子儿茶素没食子酸酯对脂多糖诱导的肝毒性的保护作用:对Hep3B细胞的体外研究

The protective effects of epigallocatechin gallate on lipopolysa ccharide-induced hepatotoxicity: an in vitro study on Hep3B cells.

作者信息

Karamese Murat, Guvendi Bulent, Karamese Selina Aksak, Cinar Irfan, Can Serpil, Erol Huseyin Serkan, Aydin Hakan, Gelen Volkan, Karakus Emre

机构信息

Department of Medical Microbiology, Medical Faculty, Kafkas University, Kars, Turkey.

Department of General Surgery, Medical Faculty, Kafkas University, Kars, Turkey.

出版信息

Iran J Basic Med Sci. 2016 May;19(5):483-9.

Abstract

OBJECTIVES

In the present study, our aim was to investigate the possible protective effects of epigallocatechin gallate (EGCG) on lipopolysaccharide (LPS)-induced hepatotoxicity by using Hep3B human hepatoma cells. Specifically, the study examines the role of some proinflammatory markers and oxidative damage as possible mechanisms of LPS-associated cytotoxicity. Consequently, the hepatocellular carcinoma cell line Hep3B was chosen as a model for investigation of LPS toxicity and the effect of EGCG on LPS-exposed cells.

MATERIALS AND METHODS

The Hep3B human hepatoma cells were used for this study. The cytotoxic effects of chemicals (EGCG and LPS), AST and ALT levels, SOD and CAT activities, GSH-Px level and TNF-alpha and IL-6 levels were detected by using different biochemical and molecular methods. LPS and EGCG were applied to cells at various times and doses.

RESULTS

The highest treatment dose of EGCG (400 µM) led to a dramatic decrease in SOD level and increase in CAT and GSH levels. Additionally, the highest dose of EGCG also led to a dramatic increase in TNF-alpha and IL-6 levels. On the other hand, effective doses of EGCG (200 and 100 µM) normalized all related parameters levels.

CONCLUSION

LPS caused hepatotoxicity, but interestingly, a high dose of EGCG was found to be a cytotoxic agent in this study. However, other two doses of EGCG led to a decrease in both inflammatory cytokine levels and antioxidant enzyme levels. Further studies should examine the effect of EGCG on secondary cellular signaling pathways.

摘要

目的

在本研究中,我们的目的是通过使用Hep3B人肝癌细胞来研究表没食子儿茶素没食子酸酯(EGCG)对脂多糖(LPS)诱导的肝毒性的可能保护作用。具体而言,该研究考察了一些促炎标志物和氧化损伤作为LPS相关细胞毒性可能机制的作用。因此,选择肝癌细胞系Hep3B作为研究LPS毒性及EGCG对LPS暴露细胞影响的模型。

材料与方法

本研究使用Hep3B人肝癌细胞。通过不同的生化和分子方法检测化学物质(EGCG和LPS)的细胞毒性作用、天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)水平、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性、谷胱甘肽过氧化物酶(GSH-Px)水平以及肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)水平。在不同时间和剂量下将LPS和EGCG应用于细胞。

结果

EGCG的最高处理剂量(400μM)导致SOD水平显著降低,CAT和GSH水平升高。此外,EGCG的最高剂量还导致TNF-α和IL-6水平显著升高。另一方面,EGCG的有效剂量(200和100μM)使所有相关参数水平恢复正常。

结论

LPS导致肝毒性,但有趣的是,在本研究中发现高剂量的EGCG是一种细胞毒性剂。然而,其他两个剂量的EGCG导致炎症细胞因子水平和抗氧化酶水平均降低。进一步的研究应考察EGCG对二级细胞信号通路的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a73c/4923468/bee1d0589283/IJBMS-19-483-g001.jpg

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