evodine has been researched along with rutecarpine* in 4 studies
1 trial(s) available for evodine and rutecarpine
Article | Year |
---|---|
Anti-inflammatory activity in skin by biomimetic of Evodia rutaecarpa extract from traditional Chinese medicine.
Wu-Zhu-Yu, is an extract prepared from the small berry fruit of Evodia rutaecarpa and is reported to have anti-inflammatory and anti-nociceptic activity. Methyl nicotinate (MN) is known to induce the release of PGD(2) resulting in localized erythema within 30 min after topical application to human skin.. The purpose of this study was to determine if a defined biomimetic mixture of components of Evodia fruit extract inhibit inflammation in human cells and skin.. In order to control the potency of the test article, we prepared a defined biomimetic mixture of synthetic and natural forms of the active components of Evodia fruit extract, containing rutaecarpine, dehydroevodiamine, and evodin. This was tested for anti-inflammatory activity in UVB-irradiated cultured cells and in the MN model of micro-inflammation in human skin.. This Evodia biomimetic mixture was a potent inhibitor of UVB-induced PGE(2) released by keratinocytes in culture. We found that MN also induces release of nitric oxide from cultured keratinocytes and microvascular endothelial cells. Twice daily application of 0.1-1% Evodia biomimetic mixture for 2 weeks significantly inhibited erythema after a MN challenge. A single application of 1% Evodia biomimetic mixture also significantly inhibited MN-induced erythema when applied at 60 min before, or within 5 min after MN exposure. The Evodia biomimetic mixture was significantly more effective at inhibiting erythema than bisabolol, the active component of chamomile.. These results demonstrate that compounds found in E. rutaecarpa (including the indole quinazoline alkaloids) have powerful anti-inflammatory activity when applied topically to human skin. Topics: Administration, Cutaneous; Adult; Alkaloids; Anti-Inflammatory Agents; Biomimetics; Cell Line; Dinoprostone; Dose-Response Relationship, Drug; Drugs, Chinese Herbal; Erythema; Evodia; Furans; Heterocyclic Compounds, 4 or More Rings; Humans; Indole Alkaloids; Keratinocytes; Middle Aged; Nicotinic Acids; Nitric Oxide; Plant Extracts; Quinazolines; Skin; Time Factors; Ultraviolet Rays | 2006 |
3 other study(ies) available for evodine and rutecarpine
Article | Year |
---|---|
Toxicity of Evodiae fructus on rat liver mitochondria: the role of oxidative stress and mitochondrial permeability transition.
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 |
[Assay of evodin, evodiamine and rutaecarpine in Fructus Evodiae by QAMS].
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.
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 |