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首页> 外文期刊>Life sciences >Cysteine aggravates palmitate-induced cell death in hepatocytes.
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Cysteine aggravates palmitate-induced cell death in hepatocytes.

机译：半胱氨酸加剧肝细胞中的棕榈酸盐诱导的细胞死亡。

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摘要

AIMS: Lipotoxicity, defined as cell death induced by excessive fatty acids, especially saturated fatty acids, is critically involved in the development of non-alcoholic steatohepatitis (NASH). Recent studies report that plasma cysteine concentrations is elevated in the subjects with either alcoholic steatohepatitis (ASH) or NASH than normal subjects. The present study was conducted to determine if elevation of cysteine could be a deleterious factor in palmitate-induced hepatocyte cell death. MAIN METHODS: HepG2 and Hep3B cells were treated with palmitate with/without the inclusion of cysteine in the media for 24h. The effects of cysteine inclusion on palmitate induced cell death were determined by lactate dehydrogenase (LDH) release and MTT assay. Oxidative stress was evaluated by intracellular glutathione (GSH) level, malondialdehyde (MDA) formation, and DCFH-DA assay. Western blotting was performed to detect the changes of endoplasmic reticulum(ER) stress markers: C/EBP homologous transcription factor (CHOP), GRP-78, and phosphorylated c-jun N-terminal kinase (p-JNK). KEY FINDINGS: Elevated intracellular cysteine aggravates hepatocytes to palmitate-induced cell death. Enhancement of ER stress, specifically increased activation of JNK pathway, contributed to this cell death process. SIGNIFICANCE: Increase of plasma cysteine levels, as observed in both ASH and NASH patients, may play a pathological role in the development of the liver diseases. Manipulation of dietary amino acid supplementation could be a therapeutic choice.
机译：目的：脂毒性，定义为通过过量脂肪酸，尤其是饱和脂肪酸引起的细胞死亡，批判性地参与非酒精脱脂性肝炎（NASH）的发育。最近的研究报告说，血浆半胱氨酸浓度升高于受欢迎的受试者中，具有比正常对象的酒精脱脂性炎（灰）或纳什升高。进行本研究以确定半胱氨酸的升高是否可能是棕榈酸诱导的肝细胞死亡中的有害因素。主要方法：HepG2和Hep3B细胞用棕榈酸盐处理/不包含培养基中的半胱氨酸24小时。通过乳酸脱氢酶（LDH）释放和MTT测定法测定半胱氨酸含有对棕榈酸诱导的细胞死亡的影响。通过细胞内谷胱甘肽（GSH）水平，丙二醛（MDA）形成和DCFH-DA测定评估氧化应激。进行蛋白质印迹以检测内质网（ER）应激标记物的变化：C / EBP同源转录因子（Chec），GRP-78和磷酸化C-JUM N-末端激酶（P-JNK）。主要发现：升高的细胞内半胱氨酸加重肝细胞对棕榈酸酯诱导的细胞死亡。 ER应激的增强，特别是JNK途径的激活，有助于这种细胞死亡过程。意义：血浆半胱氨酸水平的增加，如灰和纳什患者所述，可能在肝脏疾病的发展中发挥病理作用。膳食氨基酸补充的操纵可能是治疗性的选择。

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  • 来源
    《Life sciences》 |2011年第24期|共8页
  • 作者

    Dou X; Wang Z; Yao T; Song Z;

  • 作者单位

    College of Life Science Zhejiang Chinese Medical University Hangzhou Zhejiang 310053 PR China.;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医药、卫生;
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