Wikipedia
Linking: http://en.wikipedia.org/wiki/Evodiamine
Evodiamine, a major alkaloidal principle of Evodia fruits (Evodia rutaecarpa,
Rutaceae), showed vanilloid receptor agonistic activities comparable to
capsaicin. The Chinese literature refers to Evodia fruits as a "hot nature"
herb. In spite of the similarities in the actions of evodiamine and capsaicin in
vitro, evodiamine has no perceptible taste, including a peppery hot taste.
Therefore, the effectiveness of evodiamine and the extract of Evodia fruits in
preventing obesity on male C3H mice, or male SD rats were examined. When
evodiamine was supplemented at 0.03% of the diet and fed to mice for 12 days,
the perirenal fat weight became significantly lower than in the control group. (http://www.ncbi.nlm.nih.gov/)
Traditional Chinese herbs are regarded as a new and promising source of
potential anti-cancer remedies and new chemotherapy adjuvants to enhance the
efficacy of chemotherapy and/or to ameliorate its side effects. Extensive
investigations have been undertaken both in the experimental and clinical
studies over the years to augment the efficacy of chemotherapy. Evodia
rutaecarpa is a very popular multi-purpose herb traditionally used in
China for the treatment of headaches, abdominal pain, postpartum hemorrhage,
dysentery and amenorrhea. The major constituents of Evodia rutaecarpa are
evodiamine and rutaecarpine. Growing evidence demonstrates that evodiamine
possesses anti-cancer activities both in vitro and in vivo by
inhibiting proliferation, invasion and metastasis, inducing apoptosis of a
variety of tumor cell lines. This review is aimed to summarize the recent
researches on evodiamine focusing on anti-cancer activity and to highlight
molecular mechanisms during the past ten years. (http://www.mdpi.com/
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. (http://sciencelinks.jp/)
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