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Cytotoxicity of Abnormal Savda Munziq aqueous extract in human hepatoma (HepG2) cells
Author(s) -
Yusup Abdiryim,
Upur Halmurat,
Baudrimont Isabelle,
Umar Anwar,
Kader Turghun,
Begaud Bernard,
Creppy Edmond E.,
Moore Nicholas
Publication year - 2005
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2005.00342.x
Subject(s) - lipid peroxidation , cytotoxicity , lactate dehydrogenase , thiobarbituric acid , viability assay , biochemistry , malondialdehyde , chemistry , microbiology and biotechnology , betulinic acid , uridine , thymidine , pharmacology , antioxidant , dna , in vitro , rna , biology , enzyme , genetics , gene
Abnormal Savda Munziq (ASMq) is a traditional Uighur medicinal herbal preparation commonly used to treat diseases such as diabetes, cardiovascular diseases, chronic asthma and especially digestive cancer. Earlier studies have shown that ASMq is a free radical scavenger and could prevent mitochondrial and DNA oxidative damage. In this study, we tested the effects of aqueous extract of ASMq on human hepatoma cells (HepG2) to explore the possible mechanism of its putative anticancer properties. Aqueous extract of ASMq was tested on HepG2 proliferation (MTT assay) at 72 h, cell viability at 48 h (neutral red assay), lactate dehydrogenase release over 48 or 72 h as a measure of cytoplasmic leakage, lipid peroxidation (malondialdehyde–thiobarbituric acid adducts) at 48 h, and incorporation of [ 3 H]‐leucine, [ 3 H]‐thymidine and [ 3 H]‐uridine into cellular protein, DNA and RNA, respectively, at 24 or 48 h to assess the inhibition effects to cellular macromolecule synthesis. Our results showed a significant ( P < 0.05) time‐ and concentration‐dependent inhibition of HepG2 proliferation and viability, with increased cytoplasmic leakage, and time‐ and concentration‐dependent inhibition of protein, DNA and RNA synthesis. No lipid peroxidation was found at these concentrations. The results of the present study suggest that the putative anticancer mechanisms of ASMq may at least involve cytotoxicity.