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T-2毒素致猪肾细胞损伤及氧化应激相关机理的研究
引用本文:熊款款,吴映欣,易思亮,杨凌宸.T-2毒素致猪肾细胞损伤及氧化应激相关机理的研究[J].中国畜牧兽医,2021,48(12):4710-4717.
作者姓名:熊款款  吴映欣  易思亮  杨凌宸
作者单位:湖南农业大学动物医学院, 长沙 410128
基金项目:国家自然科学基金青年基金项目(31802252);湖南省教育厅优秀青年项目(18B113)
摘    要:试验旨在研究T-2毒素对猪肾细胞(PK15)的毒性作用及其氧化应激反应。用不同浓度的T-2毒素处理细胞,通过MTT法检测细胞活性、测定细胞内乳酸脱氢酶(LDH)释放率及苏木素伊红(HE)染色观察细胞形态变化评估T-2毒素对细胞的毒性作用;通过检测细胞内的活性氧(ROS)水平、丙二醛(MDA)含量及谷胱甘肽(GSH)含量、谷胱甘肽过氧化物酶(GPx)活性,评估不同剂量T-2毒素对细胞氧化应激水平的影响;检测Nrf2-ARE信号通路相关基因Nrf2、Keap1、GPx-1、Nqo1及Hmox1 mRNA的表达水平,分析T-2毒素对该信号通路的影响。结果表明,PK15细胞活性呈毒素剂量依赖性下降(P<0.05),LDH释放率呈毒素剂量依赖性上调(P<0.05);随T-2毒素剂量升高,细胞间隙逐渐增加,细胞固缩,细胞数量也随之减少。细胞内ROS阳性细胞率呈剂量依赖性升高,且T-2毒素为100 nmol/L时,ROS阳性细胞率显著高于其他剂量组(P<0.05);细胞内MDA含量与GPx活性呈毒素剂量依赖性升高(P<0.05),而GSH含量呈毒素剂量依赖性下降(P<0.05)。20、50及100 nmol/L的T-2毒素可显著上调Keap1、Gpx-1及Nqo1基因mRNA的相对表达量(P<0.05),且50 nmol/L的相对表达量最高。T-2毒素对K15细胞有毒性作用,可诱导其氧化损伤,且该氧化应激过程受Nrf2-AER信号通路调控。

关 键 词:T-2毒素  PK15细胞  毒性作用  氧化应激  Nrf2-ARE通路  
收稿时间:2021-05-27

Mechanism of T-2 Toxin Induced Injury and Oxidative Stress in PK15 Cells
XIONG Kuankuan,WU Yingxin,YI Siliang,YANG Lingchen.Mechanism of T-2 Toxin Induced Injury and Oxidative Stress in PK15 Cells[J].China Animal Husbandry & Veterinary Medicine,2021,48(12):4710-4717.
Authors:XIONG Kuankuan  WU Yingxin  YI Siliang  YANG Lingchen
Institution:College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, China
Abstract:The purpose of this test was to study the toxic effect of T-2 toxin on porcine kidney cells (PK15) and its oxidative stress response.The cells were treated with different concentrations of T-2 toxin.The cytotoxicity of the toxin was evaluated by MTT assay, intracellular lactate dehydrogenase (LDH) release rate and HE staining.The effects of different doses of T-2 toxin on the level of oxidative stress were evaluated by detecting the levels of reactive oxygen species (ROS), malondialdehyde (MDA), total glutathione (GSH) and total glutathione peroxidase (GPx).The expression levels of Nrf2, Keap1, GPx-1, Nqo1 and Hmox1 genes mRNA related to Nrf2-ARE signal pathway were detected, and the effect of T-2 toxin on this signal pathway was analyzed.The results showed that the activity of PK15 cells decreased in a toxin dose-dependent manner (P<0.05), and the release rate of LDH increased in a toxin dose-dependent manner (P<0.05).With the increase of T-2 toxin dose, the cell gap gradually increased, the cell pyknosis and the number of cells decreased.The rate of ROS positive cells increased in a dose-dependent manner, and when T-2 toxin was 100 nmol/L, the rate of ROS positive cells was significantly higher than that in other dose groups (P<0.05).The intracellular MDA content and GPx activity increased in a toxin dose-dependent manner (P<0.05), while the GSH content decreased in a toxin dose-dependent manner (P<0.05).20, 50 and 100 nmol/L T-2 toxin could significantly up regulate the relative expression of Keap1, GPx-1 and Nqo1 genes mRNA (P<0.05), and the relative expression of 50 nmol/L was the highest.T-2 toxin caused toxic effects on PK15 cells and induced oxidative damage, and the oxidative stress process was regulated by Nrf2-AER signal pathway.
Keywords:T-2 toxin  PK15 cells  toxicity  oxidative stress  Nrf2/ARE pathway  
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