中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (24): 4432-4436.doi: 10.3969/j.issn.1673-8225.2011.24.015

• 组织构建与生物活性因子 tissue construction and bioactive factors • 上一篇    下一篇

中波紫外线诱导HaCaT细胞凋亡与扇贝多肽的影响：肿瘤坏死因子α/肿瘤坏死因子受体1通路的研究

郑淞文1, 2，李金莲3，王春波1，韩彦弢1   

  1. 1青岛大学医学院药理教研室，山东省青岛市 266071
    2大连市中心医院放射科，辽宁省大连市  116011
    3滨州医学院药理教研室，山东省滨州市  256603
  • 收稿日期:2011-03-07 修回日期:2011-05-10 出版日期:2011-06-11 发布日期:2011-06-11
  • 通讯作者: 韩彦弢，博士，青岛大学医学院药理教研室，山东省青岛市 266071 cbwang666@126.com
  • 作者简介:郑淞文★，女，1980年生，山东省威海市人，汉族，青岛大学医学院在读硕士，医师，主要从事从事放射学工作。 dtdoudou@163.com
  • 基金资助:

    国家自然科学基金(30471458)。

Effect of polypeptide from Chlamys farreri on ultraviolet B radiation-induced HaCaT cell apoptosis: Tumor necrosis factor-alpha/tumor necrosis factor receptor 1 pathway

Zheng Song-wen1,2, Li Jin-lian3, Wang Chun-bo1, Han Yan-tao1   

  1. 1Department of Pharmacology, Medical College, Qingdao University, Qingdao  266071, Shandong Province, China
    2 Department of Radiology,Dalian Municipal Central Hospital, Dalian  116011, Liaoning Province, China
    3 Department of Pharmacology, Binzhou Medical University, Binzhou 256603,  Shandong Province, China
  • Received:2011-03-07 Revised:2011-05-10 Online:2011-06-11 Published:2011-06-11
  • Contact: Han Yan-tao, Doctor, Department of Pharmacology, Medical College, Qingdao University, Qingdao 266071, Shandong Province, China cbwang666@126.com
  • About author:Zheng Song-wen, Studying for master’s degree, Physician, Department of Pharmacology, Medical College, Qingdao University, Qingdao 266071, Shandong Province, China; Department of Radiology ,Dalian Municipal Central Hospital, Dalian 116011, Liaoning Province, China dtdoudou@163.com
  • Supported by:

    the National Natural Science Foundation of China, No. 30471458*

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摘要：

背景：扇贝多肽可以通过Fas通路及NF-κB通路发挥对中波紫外线照射后的人角质形成细胞株(HaCaT)的保护作用。
目的：观察中波紫外线辐射后HaCaT细胞的凋亡情况和细胞内肿瘤坏死因子α/肿瘤坏死因子受体1的活化情况，以及扇贝多肽的干预作用。
方法：实验以20 mJ/cm2中波紫外线辐照HaCaT细胞0.5 h建立细胞辐射损伤模型，药物低、中、高剂量组、阳性对照组、抑制剂组分别在造模前2 h加入1.42，2.84，5.69 mmol/L的扇贝多肽、5.68 mmol/L的维生素C及50 mg/L的抗肿瘤坏死因子α单克隆抗体。
结果与结论：中波紫外线辐照后，HaCaT细胞凋亡增多，肿瘤坏死因子α、肿瘤坏死因子受体1 mRNA及磷酸化JNK蛋白表达量增加；1.42，2.84，5.69 mmol/L的扇贝多肽均可降低中波紫外线辐照引起的细胞内肿瘤坏死因子α、肿瘤坏死因子受体1 mRNA及磷酸化JNK表达，抑制HaCaT细胞凋亡，以5.69 mmol/L扇贝多肽的作用效果最明显，与5.68 mmol/L维生素C的作用相当，且50 mg/L抗肿瘤坏死因子α单克隆抗体也可明显降低中波紫外线辐照引起的细胞内磷酸化JNK表达。说明扇贝多肽能抑制中波紫外线辐照引起的HaCaT细胞凋亡，其可以通过肿瘤坏死因子α/肿瘤坏死因子受体1通路发挥抗凋亡作用。

关键词: 扇贝多肽, 肿瘤坏死因子&alpha, /肿瘤坏死因子受体1, JNK, 中波紫外线, 凋亡, HaCaT细胞

Abstract:

BACKGROUND: Polypeptide from Chlamys farreri (PCF) exerts protective effects on ultraviolet B radiation-induced human keratinocyte cell line HaCaT cells through Fas pathway and nuclear factor-κB pathway.
OBJECTIVE: To investigate HaCaT cell apoptosis after ultraviolet B radiation, and activation of tumor necrosis factor-α/ tumor necrosis factor receptor-1, and intervention of PCF.
METHODS: Cell injury models were established by 20 mJ/cm2 ultraviolet B radiation on HaCaT cells for 0.5 hour. Low-dose, moderate-dose and high-dose drug groups, positive control group and inhibitor group were treated with 1.42, 2.84, 5.69 mmol/L PCF, 5.68 mmol/L vitamin C and 50 mg/L anti- tumor necrosis factor-α monoclonal antibody.
RESULTS AND CONCLUSION: After ultraviolet B radiation, HaCaT cell apoptosis became more. Tumor necrosis factor-α, tumor necrosis factor receptor 1 mRNA and phosphorylated c-Jun N-terminal kinase expression increased. 1.42, 2.84 and 5.69 mmol/L PCF could reduce ultraviolet B radiation-induced tumor necrosis factor-α, tumor necrosis factor receptor 1 mRNA and phosphorylated c-Jun N-terminal kinase expression, and inhibit cell apoptosis, especially 5.69 mmol/L PCF, which was identical to the effects of 5.68 mmol/L vitamin C. 50 mg/L anti-tumor necrosis factor-α monoclonal antibody significantly decreased ultraviolet B radiation-induced phosphorylated c-Jun N-terminal kinase expression. These suggest that PCF inhibited ultraviolet B radiation-induced HaCaT cell apoptosis by tumor necrosis factor-α/tumor necrosis factor receptor 1 pathway.

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