4.7 Article

Chemical composition of total flavonoids from Salvia chinensia Benth and their pro-apoptotic effect on hepatocellular carcinoma cells: Potential roles of suppressing cellular NF-κB signaling

Journal

FOOD AND CHEMICAL TOXICOLOGY
Volume 62, Issue -, Pages 420-426

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2013.09.008

Keywords

Salvia chinensia Benth; Flavonoids; Hepatocellular carcinoma; Apoptosis; Nuclear factor kappa B

Funding

  1. Natural Science Foundation of China [31301147, 31200264]
  2. natural science foundation of Hubei Province [2012FFB07406]
  3. Chenguang Planning from natural science foundation of Wuhan City [2013070104010029]
  4. Chinese National Project of Twelfth Five-Year Plan for Science & Technology Support [2012BAI27B06]

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Salvia chinensia Benth (S. chinensia) is a medical plant that has been traditionally applied for centuries in the treatment of malignant diseases including hepatocellular carcinoma (HCC). However, the scientific basis underlying its anti-HCC activity has not been fully established. In this study, the chemical profiles of total flavonoids from S. chinensia (TFSC) were explored. Thirteen compounds which constituted the major components of TFSC were separated and identified. Flow cytometry analysis and caspase activity assays showed that TFSC dose-dependently induced HepG2 and Huh-7 HCC cell apoptosis. TFSC was also shown to substantially suppress NF-kappa B activity in HCC cells. Moreover, TFSC significantly repressed transplanted murine H22 ascitic hepatic cancer cell growth in vivo. Further studies revealed that TFSC induced HCC cell apoptosis and inhibited expressional levels of NF-kappa B responsive genes in transplanted tumor tissues. In addition, the toxic impact of TFSC on tumor-bearing mice was undetectable. These results indicate that TFSC induces HCC cell apoptosis both in vitro and in vivo. The suppression of cellular NF-kappa B activity is implicated in the TFSC-mediated HCC cell apoptosis. (C) 2013 Elsevier Ltd. All rights reserved.

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