...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Clinical and Diagnostic Research >Citral, A Monoterpene Protect Against High Glucose Induced Oxidative Injury in HepG2 Cell In Vitro-An Experimental Study BC10-BC15
【24h】

Citral, A Monoterpene Protect Against High Glucose Induced Oxidative Injury in HepG2 Cell In Vitro-An Experimental Study BC10-BC15

机译：柠檬醛，一种单萜防止高糖诱导的HepG2细胞氧化损伤的实验研究BC10-BC15

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Introduction: Diabetes mellitus, a major metabolic disorder associated with hyperglycaemia is one of the leading cause of death in many developed countries. However, use of natural phytochemicals have been proved to have a protective effect against oxidative damage.Aim: To investigate the effect of citral, a monoterpene on high glucose induced cytotoxicity and oxidative stress in human hepatocellular liver carcinoma (Hep G2) cell line.Materials and Methods: Cells were treated with 50 mM concentration of glucose for 24 hours incubation following citral (30 μM) was added to confluent HepG2 cells. Cell viability, Reactive Oxygen Species (ROS) generation, DNA damage, lipid peroxidation, antioxidants and Mitogen Activated Protein Kinases (MAPKs) signaling were assessed in citral and/or high glucose induced HepG2 cells.Results: Cells treated with glucose (50 mM), resulted in increased cytotoxicity, ROS generation, DNA damage, lipid peroxidation and depletion of enzymatic and non enzymatic antioxidants. In contrast, treatment with citral (30 μM) significantly decreased cell cytotoxicity, ROS generation, DNA damage, lipid peroxidation and increased antioxidants enzymes in high glucose induced HepG2 cells. In addition, the present study highlighted that high glucose treated cells showed increased expression of Extracellular Signal Regulated Protein Kinase-1 (ERK-1), c-Jun N-terminal Kinase (JNK) and p38 in HepG2 cells. On the other hand treatment with citral significantly suppressed the expression of ERK-1, JNK and p38 in high glucose induced HepG2 cells.Conclusion: Citral protects against high glucose induced oxidative stress through inhibiting ROS activated MAPK signaling pathway in HepG2 cells.
机译：简介：糖尿病是一种与高血糖症相关的主要代谢疾病，是许多发达国家的主要死亡原因之一。然而，已证明使用天然植物化学物质具有抗氧化损伤的作用。目的：研究柠檬醛，单萜对高糖诱导的人肝细胞肝癌（Hep G2）细胞系的细胞毒性和氧化应激的影响。方法：将柠檬醛（30μM）加入融合的HepG2细胞中后，用50 mM浓度的葡萄糖处理细胞24小时。在柠檬酸和/或高葡萄糖诱导的HepG2细胞中评估了细胞活力，活性氧（ROS）生成，DNA损伤，脂质过氧化，抗氧化剂和丝裂原活化的蛋白激酶（MAPK）信号转导。结果：用葡萄糖（50 mM）处理的细胞导致细胞毒性增加，ROS生成，DNA损伤，脂质过氧化以及酶和非酶抗氧化剂的消耗。相反，柠檬酸（30μM）处理可显着降低高糖诱导的HepG2细胞的细胞毒性，ROS生成，DNA损伤，脂质过氧化和抗氧化剂酶的增加。此外，本研究强调高糖处理的细胞在HepG2细胞中显示出细胞外信号调节蛋白激酶1（ERK-1），c-Jun N端激酶（JNK）和p38的表达增加。另一方面，柠檬醛能明显抑制高糖诱导的HepG2细胞中ERK-1，JNK和p38的表达。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号