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七叶皂苷钠通过CARMA3/NF-κB信号通路抑制肝癌细胞的增殖

李未祥 周大臣 王石 崔笑 侯辉 耿小平

中国药理学通报2018,Vol.34Issue(9):1243-1248,6.
中国药理学通报2018,Vol.34Issue(9):1243-1248,6.DOI:10.3969/j.issn.1001-1978.2018.09.012

七叶皂苷钠通过CARMA3/NF-κB信号通路抑制肝癌细胞的增殖

Sodium aescinate inhibits proliferation of hepatocellular carcinoma through CARMA3/NF-κB signaling pathway

李未祥 1周大臣 1王石 1崔笑 1侯辉 1耿小平1

作者信息

  • 1. 安徽医科大学第二附属医院肝胆外科,安徽 合肥 230601
  • 折叠

摘要

Abstract

Aim To investigate the expression of CAR-MA3, NF-κB in hepatocellular carcinoma tissues and the underlying mechanism of sodium aescinate in inhib-iting the proliferation of human hepatocellular carcino-ma cells. Methods The expression of CARMA3 and NF-κB in HCC tissues were detected by tissue microar-ray immunohistochemistry. MTT was used to determine the effect of sodium aescinate on the proliferation of HCC cells. Cell apoptosis was detected by flow cytom-etry. The expression of CARMA3, NF-κB protein in HepG2 and Hep3B cells treated with sodium aescinate was detected by Western blot and cell immunofluores-cence. Results Tissue microarray analysis showed that the expression of CARMA3 in HCC was up-regulated compared with the adjacent adjacent liver tissues, and the histopathological differentiation, TNM stage, tumor volume and prognosis were correlated. Sodium aesci-nate in 40 μmol·L-1concentration ( IC50) inhibited the growth of HCC cell lines, promoting its apoptosis, but without toxic effects on normal liver cells. Western blot and cell immunofluorescence detection of sodium aescinate could significantly inhibit the expression of CARMA3 and NF-κB. Conclusion Sodium aescinate can effectively inhibit the proliferation of HCC cells by inhibiting the activation of CARMA3/NF-κB signaling in HCC.

关键词

CARMA3/NF-κB/七叶皂苷钠/肝细胞癌/免疫组化/信号通路

Key words

CARMA3/NF-κB/sodium aescinate/hepatocellular carcinoma/immunohistochemistry/sig-naling pathway

分类

医药卫生

引用本文复制引用

李未祥,周大臣,王石,崔笑,侯辉,耿小平..七叶皂苷钠通过CARMA3/NF-κB信号通路抑制肝癌细胞的增殖[J].中国药理学通报,2018,34(9):1243-1248,6.

基金项目

安徽省高等学校自然科学基金资助项目 ( No KJ2017A825) ( No KJ2017A825)

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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