evodine and evodiamine

evodine has been researched along with evodiamine* in 4 studies

Other Studies

4 other study(ies) available for evodine and evodiamine

ArticleYear
Toxicity of Evodiae fructus on rat liver mitochondria: the role of oxidative stress and mitochondrial permeability transition.
    Molecules (Basel, Switzerland), 2014, Dec-16, Volume: 19, Issue:12

    Evodiae fructus (EF) has been used in China for thousands of years as an analgesic, antiemetic, anti-inflammatory and antidiarrheal drug. EF is a toxic drug and causes hepatotoxicity in humans. Although recent chronic toxicity studies performed on aqueous extract of EF has revealed that it can produce obvious cumulative hepatotoxicity, the mechanism behind this toxicity is still uncertain. In the present study, we investigated the influence of EF on oxidative stress, mitochondrial permeability transition, adenosine triphosphate (ATP), and cytochrome C release of hepatic mitochondria. Rats were divided into four groups and fed distilled water, 6, 12, 24 g/kg of aqueous extract of EF daily for 15 days. Evodiamine, rutaecarpine and evodine were quantified in the aqueous extract by high performance liquid chromatography with ultraviolet detection (HPLC/UV). The results showed that aqueous extract of EF could significantly (p < 0.05) decrease MnSOD levels to 56.50%, 46.77% and 19.67% of control group, GSH level was decreased to 74.24%, 53.97% and 47.91% of control group and MDA level was increased to 131.55%, 134.34% and 150.81% of control group in the 6, 12 and 24 g/kg groups, respectively; extract also induced mitochondria swelling, vacuolation, MPT pore opening and a significant decrease (p < 0.05) in mitochondrial potential, while ATP levels were significant decreased (p < 0.05) to 65.24%, 38.08% and 34.59% of control group in the 6, 12 and 24 g/kg groups, respectively, resulting in ATP depletion and CytC release, finally trigger cell death signaling, which are the partial hepatotoxicity mechanisms of EF.

    Topics: Adenosine Triphosphate; Animals; Cytochromes c; Evodia; Furans; Glutathione; Heterocyclic Compounds, 4 or More Rings; Indole Alkaloids; Male; Malondialdehyde; Membrane Potential, Mitochondrial; Mitochondria, Liver; Oxidative Stress; Permeability; Plant Extracts; Quinazolines; Rats; Superoxide Dismutase

2014
Simultaneous determination of evodiamine and evodine in Beagle dog plasma using liquid chromatography tandem mass spectrometry.
    Journal of Asian natural products research, 2013, Volume: 15, Issue:3

    A sensitive, rapid, and specific liquid chromatography/tandem mass spectrometry assay has been established and validated for the quantitation of evodiamine and evodine in Beagle dog plasma. Plasma samples of 0.2 ml were processed by liquid-liquid extraction with n-hexane/ethyl acetate (2:1, v/v). Chromatographic separations were done on a Symmetry C18 column (100 mm × 4.6 mm, ID, 5 μm) at 35°C with a linear gradient of methanol and 20 mM ammonium formate containing 0.2% formic acid. Evodiamine, evodine, and glibenclamide [internal standard (IS)] were ionized with an electrospray ionization source operated in positive ion mode. The MS/MS transitions were m/z 304.1 → 161.1 for evodiamine, m/z 471.2 → 425.1 for evodine, and m/z 494.1 → 369.1 for IS. Calibration curves were linear over the concentration range of 0.1-100 ng/ml for evodiamine and 0.5-500 ng/ml for evodine. The mean extraction recoveries were 88.10 ± 3.21% for evodiamine and 81.24 ± 4.07% for evodine. The intra- and inter-day precisions were less than 11.10% and 12.81%, and the accuracy was within ± 11.76% for both analytes. Evodiamine and evodine were stable during storage and analytical periods. The validated method has been successfully applied to a pharmacokinetic study of evodiamine and evodine in beagle dogs after oral administration.

    Topics: Administration, Oral; Animals; Chromatography, Liquid; Dogs; Furans; Heterocyclic Compounds, 4 or More Rings; Quinazolines; Spectrometry, Mass, Electrospray Ionization; Tandem Mass Spectrometry

2013
[Assay of evodin, evodiamine and rutaecarpine in Fructus Evodiae by QAMS].
    Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica, 2009, Volume: 34, Issue:21

    To develop a Quantitative Assay of Multi-components by Single - marker (QAMS) for simultaneous determination of three components in Fructus Evodiae, and examine the feasibility of using the relative correction factors between the different types of compounds.. Rutaecarpine was selected as the internal reference substance; the relative correction factors of evodin and evodiamine were calculated. The contents of three components in 11 batches of samples were determined by both external standard method and QAMS. The validity of the QAMS method was evaluated by comparison of their quantitative results.. No obvious differences (RSD < 5%) were found in the quantitative results of evodin and evodiamine in 11 batches of Fructus Evodiae determined by the two methods.. It is feasible and suitable to determine evodin and evodiamine in Fructus Evodiae by QAMS, and this method can be used for a certain different types of compounds.

    Topics: Chromatography, High Pressure Liquid; Drugs, Chinese Herbal; Evodia; Furans; Heterocyclic Compounds, 4 or More Rings; Indole Alkaloids; Plant Extracts; Quinazolines

2009
Evodiamine, a constituent of Evodiae Fructus, induces anti-proliferating effects in tumor cells.
    Cancer science, 2003, Volume: 94, Issue:1

    We found that evodiamine, a major alkaloidal component of Evodiae Fructus (Goshuyu in Japan), inhibited proliferation of several tumor cell lines, but had less effect on human peripheral blood mononuclear cells (PBMC). We used human cervical cancer cells, HeLa, as a model to elucidate the molecular mechanisms of evodiamine-induced tumor cell death. The results showed that evodiamine induced oligonucleosomal fragmentation of DNA in HeLa cells and increased the activity of caspase-3, but not that of caspase-1, in vitro. Both evodiamine-induced DNA fragmentation and caspase-3 activity were effectively inhibited by a caspase-3 inhibitor, z-DEVD-fmk (z-Asp-Glu-Val-Asp-fmk). In addition, evodiamine increased the expression of the apoptosis inducer Bax, but decreased the expression of the apoptosis suppressor Bcl-2 in mitochondria. Taken together, our data indicated that evodiamine alters the balance of Bcl-2 and Bax gene expression and induces apoptosis through the caspase pathway in HeLa cells.

    Topics: Alkaloids; Amino Acid Chloromethyl Ketones; Animals; Antineoplastic Agents, Phytogenic; Apoptosis; bcl-2-Associated X Protein; Caspase 3; Caspases; Cell Division; Cysteine Proteinase Inhibitors; Dactinomycin; DNA Fragmentation; Drug Screening Assays, Antitumor; Enzyme Activation; Evodia; Fibrosarcoma; Fluorouracil; Furans; Gene Expression Regulation, Neoplastic; Genes, bcl-2; HeLa Cells; Hepatocytes; Heterocyclic Compounds, 4 or More Rings; Humans; Indole Alkaloids; Leukemia, Monocytic, Acute; Leukocytes, Mononuclear; Melanoma; Mice; Mitochondria; Molecular Structure; Neoplasm Proteins; Oligopeptides; Plant Extracts; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; Quinazolines; Rats; Rats, Inbred BUF; Sarcoma 180; Tumor Cells, Cultured

2003