Disease relevance of Evodiamine

• Because several genes that regulate cellular proliferation, carcinogenesis, metastasis, and survival are regulated by nuclear factor-kappaB (NF-kappaB), we postulated that evodiamine mediates its activity by modulating NF-kappaB activation [1].
• Inhibitory effects of evodiamine on the growth of human prostate cancer cell line LNCaP [2].
• Antitumor mechanism of evodiamine, a constituent from Chinese herb Evodiae fructus, in human multiple-drug resistant breast cancer NCI/ADR-RES cells in vitro and in vivo [3].
• Protective effects of evodiamine on myocardial ischemia-reperfusion injury in rats [4].
• In the present study, the protective effects of evodiamine on cardiac anaphylaxis were examined [5].

Psychiatry related information on Evodiamine

• Furthermore, the physiological effects of evodiamine on the aged animals may implicate a potential for the treatment of erectile dysfunction [6].

High impact information on Evodiamine

• Evodiamine abolishes constitutive and inducible NF-kappaB activation by inhibiting IkappaBalpha kinase activation, thereby suppressing NF-kappaB-regulated antiapoptotic and metastatic gene expression, up-regulating apoptosis, and inhibiting invasion [1].
• In the present study, we investigated the effect of evodiamine on NF-kappaB and NF-kappaB-regulated gene expression activated by various carcinogens [1].
• Evodiamine increased tubulin polymerization as determined by the immunocytochemical and in vivo tubulin polymerization analyses [3].
• In a time- and concentration-dependent manner, evodiamine also promoted the phosphorylations of Raf-1 kinase and Bcl-2 [3].
• Evodiamine inhibited the proliferation of NCI/ADR-RES cells in a concentration-dependent manner with a GI50 of 0.59 +/- 0.11 microM [3].

Chemical compound and disease context of Evodiamine

• In the present study, we have examined whether evodiamine protects against myocardial ischemia-reperfusion injury in rats and whether the protective effects of evodiamine are related to the activation of capsaicin-sensitive sensory nerves [4].
• These findings suggest that ER and its constituents, evodiamine and rutaecarpine, may be effective for IgE-induced allergic diseases such as atopic dermatitis and rhinitis [7].
• Inhibitory effect of evodiamine on aldosterone release by Zona glomerulosa cells in male rats [8].
• Roles of SIRT1 and phosphoinositide 3-OH kinase/protein kinase C pathways in evodiamine-induced human melanoma A375-S2 cell death [9].

Biological context of Evodiamine

• A significant and concentration-dependent inhibitory effect of evodiamine on LNCaP cell growth was observed at 24 hr and persisted for 96 hr [2].
• Furthermore, we examined the influences of evodiamine on cell death and cell cycle [2].
• The flow cytometric analysis of evodiamine-treated cells indicated a block of G2/M phase and an elevated level of DNA fragmentation [2].
• L-365,260 (3R-(+)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepine-3-yl)-N'-(3-methylphenyl)-urea), a selective CCK(2) receptor antagonist, did not alter the evodiamine-induced inhibition of gastric emptying and gastrointestinal transit [10].
• On the other hand, food-sated mice subcutaneously administered 1-3 mg/kg evodiamine showed unchanged core body temperature and increased tail skin temperature by more than 5 degrees C, suggesting the increased energy expenditure by enhanced heat dissipation [11].

Anatomical context of Evodiamine

• In an in situ assay we found that evodiamine inhibited microtubule spindle formation [12].
• The roles of the endothelium, Ca2+ and K+ fluxes in the evodiamine-induced attenuation of vascular contractile responses to vasoactive agents were examined [13].
• However, the isolated ileum from evodiamine-treated mice lost its response to sensory nerve stimuli but retained its response to vagus nerve stimuli [14].
• These results suggest that the evodiamine-induced contractile response of the bronchus could be attributed to the resultant tachykinin release from sensory neurons by binding of evodiamine to vanilloid receptors [15].
• Furthermore, both lipolytic activity in the perirenal fat tissue and specific GDP binding in brown adipose tissue mitochondria, as the biological index of enhanced heat production, were significantly increased in the evodiamine fed rats [11].

Associations of Evodiamine with other chemical compounds

• Rutaecarpine, evodiamine, and dehydroevodiamine are quinazolinocarboline alkaloids isolated from a traditional Chinese medicine, Evodia rutaecarpa [16].
• In conclusion, we have demonstrated that a novel non-pungent vanilloid receptor agonist, evodiamine, mimics the characteristic anti-obese effects induced by capsaicin [11].
• The nociceptive action (paw licking behaviour) was dose dependently induced by intradermal injection (i.d.) of evodiamine to the hind paw and was suppressed by the co-treatment with capsazepine, a vanilloid receptor specific agonist, in a dose-dependent manner [14].
• The present study explored the effects of evodiamine on testosterone secretion in vitro [17].
• The vasoreactivity of dehydroevodiamine (1), evodiamine (2), and rutaecarpine (3), quinazoline alkaloids isolated from Evodia rutaecarpa, to aorta smooth muscle demonstrated that they produce a vasodilatory effect on endothelium-intact rat aorta with equal potency [18].

Gene context of Evodiamine

• After the collection of conditioned media, the VEGF expression of remaining CL1 cells were determined by Western analyses and revealed that evodiamine decreased VEGF expression [19].
• However, IL-1Ra attenuated the enhanced phosphorylation level of p38 mitogen-activated protein kinase (p38 MAPK) without affecting extracellular signal-regulated protein kinase (ERK) inactivation induced by evodiamine [20].
• 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 [21].
• After treatment with evodiamine for the indicated time periods, anti-apoptotic protein SIRT1 expression was decreased; p53 expression and its phosphorylation were both enhanced, whereas transient induction of downstream p21 was not enough to promote cell cycle arrest [9].
• In addition, evodiamine increased the expression of the apoptosis inducer Bax, but decreased the expression of the apoptosis suppressor Bcl-2 in mitochondria [21].

Analytical, diagnostic and therapeutic context of Evodiamine

• The antitumor activity of evodiamine against the human multiple-drug resistant tumor xenograft was found to be superior to that of paclitaxel [3].
• Examination of TUNEL showed that evodiamine-induced apoptosis was observed at 24 hr and extended for 72 hr [2].
• 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 [11].
• Rats were pretreated with evodiamine 10 min before the experiment, and then the left main coronary artery of rat hearts was subjected to 60 min occlusion followed by 180 min reperfusion [4].
• Intraperitoneal injections of DeHE (5-20 mg/kg) and EVO (2.5-10 mg/kg) caused a dose-related hypothermia in afebrile rats at an ambient temperature (Ta) of 20 degrees C. Because the heat production of alkaloid-injected rats did not differ from that of the controls, the hypothermic effect likely resulted from increased peripheral heat loss [22].

References