| T-2毒素激活活性氧/核转录因子-κB信号通路诱导猪空肠上皮细胞发生炎性反应 |
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| 引用本文： | 康瑞芬,王猛,沈家鲲,金晓明,李春梅.T-2毒素激活活性氧/核转录因子-κB信号通路诱导猪空肠上皮细胞发生炎性反应[J].动物营养学报,2021,33(1). |
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| 作者姓名： | 康瑞芬 王猛 沈家鲲 金晓明 李春梅 |
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| 作者单位： | 南京农业大学动物科技学院,南京 210095;南京农业大学动物科技学院,南京 210095;南京农业大学动物科技学院,南京 210095;南京农业大学动物科技学院,南京 210095;南京农业大学动物科技学院,南京 210095 |
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| 基金项目： | 国家重点研发计划(2018YFE0127300)。 |
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| 摘 要： | 本试验以猪空肠上皮细胞(IPEC-J2)为模型细胞,探讨T-2毒素诱导IPEC-J2炎性反应的影响及相关作用机制。通过四甲基偶氮唑盐(MTT)方法测定细胞活力,选择适宜的T-2毒素和N-乙酰-L-半胱氨酸(NAC)浓度。试验分为4个组,分别为对照组、NAC组(4.0 mmol/L NAC)、T-2组(4.0 ng/mL T-2毒素)和T-2+NAC组(4.0 ng/mL T-2毒素+4.0 mmol/L NAC),处理12 h后测定各组IPEC-J2中丙二醛(MDA)含量、总超氧化物歧化酶(T-SOD)和过氧化氢酶(CAT)活性、活性氧(ROS)水平、细胞炎症相关基因和核转录因子-κB(NF-κB)的相对表达量。结果表明:1)与对照组相比,T-2组IPEC-J2中CAT、T-SOD活性极显著降低(P<0.01),IPEC-J2中MDA含量和ROS水平极显著升高(P<0.01)。与T-2组相比,T-2+NAC组IPEC-J2中CAT和T-SOD活性极显著升高(P<0.01),IPEC-J2中MDA含量和ROS水平显著或极显著降低(P<0.05或P<0.01)。2)与对照组相比,T-2组IPEC-J2中肿瘤坏死因子-α(TNF-α)(P<0.05)、白细胞介素-6(IL-6)(P<0.01)、白细胞介素-10(IL-10)(P>0.05)的mRNA相对表达量升高。3)与对照组相比,T-2组IPEC-J2中NF-κB蛋白相对表达量极显著升高(P<0.01)。与T-2组相比,T-2+NAC组IPEC-J2中NF-κB蛋白相对表达量极显著降低(P<0.01)。由此可见,T-2毒素通过诱导IPEC-J2产生过量的ROS,促进炎症相关基因及NF-κB蛋白的表达,导致IPEC-J2发生炎性反应。
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| 关 键 词： | T-2毒素 猪空肠上皮细胞 活性氧 炎性反应 |
T-2 Toxin Induced Inflammatory Response of Intestinal Porcine Epithelial Cells by Activating Reactive Oxygen Species/Nuclear Factor-κB Signaling Pathway |
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| KANG Ruifen,WANG Meng,SHEN Jiakun,JIN Xiaoming,LI Chunmei.T-2 Toxin Induced Inflammatory Response of Intestinal Porcine Epithelial Cells by Activating Reactive Oxygen Species/Nuclear Factor-κB Signaling Pathway[J].Acta Zoonutrimenta Sinica,2021,33(1). |
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| Authors: | KANG Ruifen WANG Meng SHEN Jiakun JIN Xiaoming LI Chunmei |
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| Institution: | (College of Animal Science and Technology,Nanjing Agricultural University,Nanjing 210095,China) |
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| Abstract: | This experiment used the intestinal porcine epithelial cells(IPEC-J2)as model cells,to investigate the effects of T-2 toxin induced inflammatory response in IPEC-J2 and its related mechanism.The cell viability was measured by methyl thiazolyl tetrazolium(MTT)method,and the appropriate concentrations of T-2 toxin and N-acetyl-L-cysteine(NAC)were selected.The experiment was divided into four groups,which were control group,NAC group(4.0 mmol/L NAC),T-2 group(4.0 ng/mL T-2 toxin)and T-2+NAC group(4.0 ng/mL T-2 toxin 4.0 mmol/L NAC),respectively.After 12 h treatment,the malondialdehyde(MDA)content,total superoxide dismutase(T-SOD)activity,catalase(CAT)activity,reactive oxygen species(ROS)level and relative expression of inflammation related genes and nuclear factor-κB(NF-κB)in IPEC-J2 of each group were measured.The results showed as follows:1)compared with the control group,the activities of CAT and T-SOD in IPEC-J2 of T-2 group were significantly decreased(P<0.01),and the MDA content and ROS level in IPEC-J2 were significantly increased(P<0.01).Compared with the T-2 group,the activities of CAT and T-SOD in IPEC-J2 of T-2+NAC group were significantly increased(P<0.01),and the MDA content and ROS level in IPEC-J2 were significantly decreased(P<0.05 or P<0.01).2)Compared with the control group,the mRNA relative expressions of tumor necrosis factor-α(TNF-α)(P<0.05),interleukin-6(IL-6)(P<0.01)and interleukin-10(IL-10)(P>0.05)in IPEC-J2 of T-2 group were increased.3)Compared with the control group,the protein relative expression of NF-κB in IPEC-J2 of T-2 group was significantly increased(P<0.01).Compared with the T-2 group,the protein relative expression of NF-κB in IPEC-J2 of T-2+NAC group was significantly decreased(P<0.01).In conclusion,T-2 toxin induce inflammatory response of IPEC-J2 by increasing ROS production and promoting expressions of inflammation related genes and NF-κB protein. |
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| Keywords: | T-2 toxin IPEC-J2 ROS inflammatory response |
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