Protective Effects of Aqueous Extracts of Flos lonicerae Japonicae against Hydroquinone-Induced Toxicity in Hepatic L02 Cells

Protective Effects of Aqueous Extracts of Flos lonicerae Japonicae against Hydroquinone-Induced Toxicity in Hepatic L02 Cells
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金银花水提取物对氢醌诱导的肝 L02 细胞毒性的保护作用

DOI:
10.1155/2018/4528581
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发表时间:
2018-01-01
影响因子:
--
通讯作者:
Hu, Gonghua
Hu, Gonghua
中科院分区:
生物学2区
文献类型:
--
作者:
Gao, Yanfang;Tang, Huanwen;Hu, Gonghua

文献摘要

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对苯二酚(Hydroquinone,HQ)广泛应用于食品中,是一种职业和环境污染物.虽然HQ的肝毒性已在体外和体内得到证实,但HQ诱导的肝毒性的预防尚未阐明。本研究旨在探讨金银花水提物对HQ诱导的细胞毒性的干预作用。以160 μmol/L HQ作用12 h作为细胞毒性的阳性对照,证明HQ以浓度依赖性方式降低细胞活力。与相应的HQ处理组相比,FLJ水提取物显著增加了肝L02细胞的细胞活力,并以浓度依赖性方式降低了LDH释放、ALT和AST。这一结果表明,FLJ水提取物可以保护HQ诱导的细胞毒性。HQ使肝细胞内MDA和LPO含量增加,GSH、GSH-Px和SOD活性降低。此外,水FLJ提取物显着抑制HQ刺激的氧化损伤。HQ还可促进细胞DNA双链断裂(DSB)和8-羟基-2 ′-脱氧鸟苷(8-hydroxy-2′-deoxyguanosine,8-OH)的生成,促进细胞凋亡。然而,水FLJ提取物逆转HQ诱导的DNA损伤和细胞凋亡的浓度依赖性的方式。总之,我们的研究结果表明,HQ的毒性介导的细胞内氧化应激,激活DNA损伤和凋亡。结果还证明,水溶性FLJ提取物对HQ诱导的肝L02细胞毒性具有保护作用。
Hydroquinone (HQ) is widely used in food stuffs and is an occupational and environmental pollutant. Although the hepatotoxicity of HQ has been demonstrated both in vitro and in vivo, the prevention of HQ-induced hepatotoxicity has yet to be elucidated. In this study, we focused on the intervention effect of aqueous extracts of Flos lonicerae Japonicae (FLJ) on HQ-induced cytotoxicity. We demonstrated that HQ reduced cell viability in a concentration-dependent manner by administering 160 μmol/L HQ for 12 h as the positive control of cytotoxicity. The aqueous FLJ extracts significantly increased cell viability and decreased LDH release, ALT, and AST in a concentration-dependent manner compared with the corresponding HQ-treated groups in hepatic L02 cells. This result indicated that aqueous FLJ extracts could protect the cytotoxicity induced by HQ. HQ increased intracellular MDA and LPO and decreased the activities of GSH, GSH-Px, and SOD in hepatic L02 cells. In addition, aqueous FLJ extracts significantly suppressed HQ-stimulated oxidative damage. Moreover, HQ promoted DNA double-strand breaks (DSBs) and the level of 8-hydroxy-2′-deoxyguanosine and apoptosis. However, aqueous FLJ extracts reversed HQ-induced DNA damage and apoptosis in a concentration-dependent manner. Overall, our results demonstrated that the toxicity of HQ was mediated by intracellular oxidative stress, which activated DNA damage and apoptosis. The findings also proved that aqueous FLJ extracts exerted protective effects against HQ-induced cytotoxicity in hepatic L02 cells.