Antitumor effects of chi-shen extract from Salvia miltiorrhiza and Paeoniae radix on human hepatocellular carcinoma cells.

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  • Author(s): Hu S;Hu S; Chen SM; Li XK; Qin R; Mei ZN
  • Source:
    Acta pharmacologica Sinica [Acta Pharmacol Sin] 2007 Aug; Vol. 28 (8), pp. 1215-23.
  • Publication Type:
    Duplicate Publication; Journal Article
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Nature Publishing Group Country of Publication: United States NLM ID: 100956087 Publication Model: Print Cited Medium: Print ISSN: 1671-4083 (Print) Linking ISSN: 16714083 NLM ISO Abbreviation: Acta Pharmacol Sin Subsets: MEDLINE
    • Publication Information:
      Publication: 2009- : New York : Nature Publishing Group
      Original Publication: Beijing, China : Science Press, c2000-
    • Subject Terms:
      Antineoplastic Agents, Phytogenic/*isolation & purification ; Antineoplastic Agents, Phytogenic/*pharmacology ; Apoptosis/*drug effects ; Paeonia/*chemistry ; Plant Preparations/*pharmacology ; Salvia miltiorrhiza/*chemistry; Carcinoma, Hepatocellular/drug therapy ; Cell Cycle ; Cell Line, Tumor ; Cell Survival/drug effects ; Genes, bcl-2 ; Genes, p53 ; Humans ; Liver Neoplasms/drug therapy ; Transcription, Genetic ; bcl-2-Associated X Protein/genetics
    • Abstract:
      Aim: To investigate the antihepatocellular carcinoma effects of chi-shen extract (CSE) from the water-soluble compounds of Salvia miltiorrhiza and Paeoniae radix.
      Methods: The effect of CSE on the growth of HepG2 cells (hepatocellular carcinoma cell line) was studied by 3-(4,5)-2,5-diphenyltetrazolium bromide assay. Apoptosis were detected through acridine orange (AO) and ethylene dibromide (EB) staining and DNA fragmentation assay. The effect of CSE on the cell cycle of HepG2 cells was studied by the propidium iodide staining method. The activation of caspases-3, -8 and -9 was examined by immunoassay kits. The transcription of the Bcl-2 family and p53 was detected by RT-PCR.
      Results: Our data revealed that CSE strongly induced HepG2 cell death in a dose- and time-dependent manner. CSE-induced cell death was considered to be apoptotic by observing the typical apoptotic morphological change by AO/EB staining and DNA fragmentation assay. The induction of HepG2 cell death was caused by an induction of apoptosis for the sub-G1 proportion increase, the downregulation of Bcl-2, the upregulation of Bax and p53, and the activation of the caspases-3 and -9 pathways.
      Conclusion: These results clearly demonstrated that CSE was able to inhibit the proliferation of HepG2 cells and cause apoptosis. Moreover, the anticancer effects of CSE were related to the Bcl-2 family pathway and the activation of caspases-3 and -9 in HepG2 cells.
    • Comments:
      Comment in: Acta Pharmacol Sin. 2007 Oct;28(10):1705. (PMID: 17977096)
    • Accession Number:
      0 (Antineoplastic Agents, Phytogenic)
      0 (Plant Preparations)
      0 (bcl-2-Associated X Protein)
    • Publication Date:
      Date Created: 20070721 Date Completed: 20081118 Latest Revision: 20070720
    • Publication Date:
      20240628
    • Accession Number:
      10.1111/j.1745-7254.2007.00606.x
    • Accession Number:
      17640485