The vasorelaxant effect of evodiamine in rat isolated mesenteric arteries: mode of action

Chiou, Wen-Fei; Chou, Cheng‐Jen; Shum, Andrew Yau‐Chik; Chen, Chieh-Fu

doi:10.1016/0014-2999(92)90039-7

Cited by 98 publications

(71 citation statements)

References 19 publications

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“…Previous studies indicated that evodiamine indeed affects many physiological functions and might be a helpful medicine in the future. [21][22][23][24] Our study demonstrated that evodiamine inhibited the proliferation of androgen-dependent prostate cancer cells, LNCaP. Several studies reported that evodiamine exhibited various biological effects.…”

Section: Effects Of Evodiamine On Caspase Processingmentioning

confidence: 55%

“…It has been demonstrated that evodiamine influences many physiological functions including vasotension, anoxia and body temperature. [21][22][23] Meanwhile, evodiamine exhibits an anti-inflammatory effect on change of nitric oxide production in murine macrophage. 24 Recently, we found that evodiamine inhibited testosterone production via a decrease of 17␤-hydroxysteroid dehydrogenase activity in testicular interstitial cells.…”

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confidence: 99%

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Inhibitory effects of evodiamine on the growth of human prostate cancer cell line LNCaP

Kan¹,

Huang

Lin

et al. 2004

Intl Journal of Cancer

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Key words: prostate cancer; evodiamine; cell growth; G2/M arrest; apoptosisProstate cancer is the most commonly diagnosed malignancy in American men over 40 years of age and is the second leading of cancer deaths. 1,2 Recently, prostate cancer has become more and more common in Asia including Taiwan. 3 According to previous studies, widely accepted risk factors for prostate cancer are age, race, ethnicity, dietary habits, androgen production and metabolism. 4 Prostate cancer is characterized by an initial androgen dependency in which the growth of cancer is enhanced by androgen. 5 In this stage, treatment is aimed at either lowering the plasma level of testosterone or inhibiting its biological effects or those of its metabolites at the target tissue levels. Orchidectomy, LHRH agonists and antiandrogenic drugs have been used clinically for treatment of androgen-dependent prostate cancer. 6 -8 However, these therapies cause psychological and physiological side effects. 9 -11 The drugs for androgen-dependent prostate cancer have merits and limitations. Because of the side effects and limitations of the currently available treatments, there is a need to identify and develop new antitumor agents against androgen-dependent prostate cancer.It has been demonstrated that several microchemicals that are isolated from herbs and plants with diversified pharmacological properties exert inhibitory effects on the proliferation of cancer. [12][13][14][15][16] The microchemicals could be the most desirable agents for prevention or intervention of human cancer incidence and mortality due to stomach, colon, breast, esophagus, lung, bladder and even prostate carcinoma. [17][18][19] Our previous studies showed that cardiac glycosides from digitalis and Chansu exhibited the antiproliferative effects on prostate cancer cells including DU145, PC3 and LNCaP to mediate the elevated [Ca2 ϩ ] i and apoptosis. 19,20 Wu-Chu-Yu is a long-standing Chinese herb used for syndromes characterized by cold hands and gastrointestinal disorders. Evodiamine is one of the major bioactive compounds isolated and purified from Wu-Chu-Yu. It has been demonstrated that evodiamine influences many physiological functions including vasotension, anoxia and body temperature. [21][22][23] Meanwhile, evodiamine exhibits an anti-inflammatory effect on change of nitric oxide production in murine macrophage. 24 Recently, we found that evodiamine inhibited testosterone production via a decrease of 17␤-hydroxysteroid dehydrogenase activity in testicular interstitial cells. 25 Interestingly, the evidence showed that rutaecarpine, the other bioactive compound isolated from Wu-Chu-Yu, inhibited the growth of many kinds of cancers including breast, lung and kidney cancers. 26 Furthermore, Okasawara et al. 27,28 reported that evodiamine inhibited the cell proliferation, cell migration and lung metastasis of murine colon cancer cells.According to previous reports, evodiamine has been recognized as a compound for anti-metastatic and anti-tumor agent in colon cancer cells. It w...

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Section: Effects Of Evodiamine On Caspase Processingmentioning

confidence: 55%

mentioning

confidence: 99%

Inhibitory effects of evodiamine on the growth of human prostate cancer cell line LNCaP

Kan¹,

Huang

Lin

et al. 2004

Intl Journal of Cancer

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“…

Interleukin 1 (IL-1) is one of the multifunctional cytokines produced predominantly by activated monocytes and macrophages.

9) Among the IL-1 family, IL-1a and IL-1b are referred to be "agonist" molecules that exert not only pleiotropic effects in host reactions such as immune defence, inflammation and homeostasis, 10,11) but also regulates a variety of cell functions of many cell types in both positive and negative manners.

12-15) However, the third member IL-1 receptor antagonist (IL-1Ra) binds to the same receptors as IL1a or b, but does not induce any intracellular signal, therefore, acts as a natural inhibitor of IL-1.

11) Previous studies reported that IL-1 induced growth inhibition in human melanoma cells through down-regulation of ornithine decarboxylase (ODC), 16,17) up-regulation of IL-6 18) and cell cycle arrest.

…”

mentioning

confidence: 99%

“…Evodiamine, a constituent isolated from the dried, unripe fruit of Evodia rutaecarpa BENTHAM (go-shu-yu in Japanese) has been reported to present bronchial contractive, 1) catecholamine secretory, 2) vasodilatory, 3,4) anti-nociceptive 5) and antitumor effect.…”

mentioning

confidence: 99%

Evodiamine Induced Human Melanoma A375-S2 Cell Death Partially through Interleukin 1 Mediated Pathway

Che

Wang

Tashiro

et al. 2005

Biological & Pharmaceutical Bulletin

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Evodiamine, a constituent isolated from the dried, unripe fruit of Evodia rutaecarpa BENTHAM (go-shu-yu in Japanese) has been reported to present bronchial contractive, 1) catecholamine secretory, 2) vasodilatory, 3,4) anti-nociceptive 5) and antitumor effect.6) It was also reported that evodiamine had an inhibitory effect on tumor cell migration in vitro.7) Our previous study showed that up-regulation of Bax/Bcl-2 amplified the activation of caspase cascade, resulting in apoptosis in A375-S2 cells. Additionally, simultaneous activation of p38 mitogen-activated protein kinase (MAPK) and inhibition of extracellular signal-regulated protein kinase (ERK) activity contributed to evodiamine-induced necrosis at later stage. 8)Interleukin 1 (IL-1) is one of the multifunctional cytokines produced predominantly by activated monocytes and macrophages.9) Among the IL-1 family, IL-1a and IL-1b are referred to be "agonist" molecules that exert not only pleiotropic effects in host reactions such as immune defence, inflammation and homeostasis, 10,11) but also regulates a variety of cell functions of many cell types in both positive and negative manners.12-15) However, the third member IL-1 receptor antagonist (IL-1Ra) binds to the same receptors as IL1a or b, but does not induce any intracellular signal, therefore, acts as a natural inhibitor of IL-1.11) Previous studies reported that IL-1 induced growth inhibition in human melanoma cells through down-regulation of ornithine decarboxylase (ODC), 16,17) up-regulation of IL-6 18) and cell cycle arrest. 19) Research carried out by Itoh and his coworkers also indicated that this antiproliferative effect was mediated by p38 MAPK. 20) Our study has further confirmed that induction of Fas-ligand (Fas-L), activation of caspases, regulation of Bcl-2 family proteins and induction of endogenous IL-1b also contributed to IL-1b-induced A375-S2 cell death (data not shown). Therefore, there seem to be some similarities between evdiamine's and IL-1's anti-tumor machinery.Engagement of the extracellular domain of Fas by the Fas-L results in intracellular recruitment of caspase-8 to Fas via the adaptor protein, Fas-associated death domain (FADD) protein, because FADD interacts with Fas through its death domain and with caspase-8 through a death effector domain.21) Activation of caspase cascade was responsible for the consequent process that couples DNA damage and p53 activation to pro-or anti-apoptotic machinery involves in the Bcl-2 family proteins.8,22) Bcl-2 family was known to play essential roles in DNA damage-induced apoptosis. 23,24) In addition, p53 induction increases pro-apoptotic Bax synthesis 25) and activates Ras/Raf/MAPK cascade. 26)In the present study, we demonstrated that evodiamine induced A375-S2 melanoma cell death partially through IL-1 mediated pathway. Human melanoma is the most aggressive form of skin cancer and is becoming resistant to all current modalities of cancer therapy. The major aim of our study is to find out new target of natural product and develop specific ...

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“…Evodiamine has been shown to have various effects on biological processes, such as testosterone [28] and catecholamine secretion [29] , as well as vasodilative [30] , anti-nociceptive [31] , obesity [20] , and thermoregulatory and uterotonic effects [32] . Evodiamine has anti-tumor potential through its ability to inhibit proliferation, induce apoptosis and reduce invasion and metastasis of a wide variety of tumor cells, including breast cancer, prostate cancer, leukemic T-lymphocyte, melanoma, cervical cancer, colon cancer and lung cancer cells [33] .…”

Section: Discussionmentioning

confidence: 99%

Evodiamine improves congnitive abilities in SAMP8 and APPswe/PS1ΔE9 transgenic mouse models of Alzheimer's disease

et al. 2011

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Aim:To investigate the effect of evodiamine (a quinolone alkaloid from the fruit of Evodia rutaecarpa) on the progression of Alzheimer's disease in SAMP8 and APP swe /PS1 ΔE9 transgenic mouse models. Methods: The mice at age of 5 months were randomized into the model group, two evodiamine (50 mg·kg -1 ·d -1 and 100 mg·kg -1 ·d -1 ) groups and an Aricept (2 mg·kg -1 ·d -1 ) group. The littermates of no-transgenic mice and senescence accelerated mouse/resistance 1 mice (SAMR1) were used as controls. After 4 weeks of treatment, learning abilities and memory were assessed using Morris watermaze test, and glucose uptake by the brain was detected using positron emission tomography/computed tomography (PET/CT). Expression levels of IL-1β, IL-6, and TNF-α in brain tissues were detected using ELISA. Expression of COX-2 protein was determined using Western blot. Results: In Morris water-maze test, evodiamine (100 mg·kg -1 ·d -1 ) significantly alleviated the impairments of learning ability and memory. Evodiamine (100 mg·kg -1 ·d -1 ) also reversed the inhibition of glucose uptake due to development of Alzheimer's disease traits in mice. Furthermore, the dose of evodiamine significantly decreased the expression of IL-1β, IL-6, TNF-α, and COX-2 that were involved in the inflammation due to Alzheimer's disease. Conclusion:The results indicate that evodiamine (100 mg·kg -1 ·d -1 ) improves cognitive abilities in the transgenic models of Alzheimer's disease.

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The vasorelaxant effect of evodiamine in rat isolated mesenteric arteries: mode of action

Cited by 98 publications

References 19 publications

Inhibitory effects of evodiamine on the growth of human prostate cancer cell line LNCaP

Inhibitory effects of evodiamine on the growth of human prostate cancer cell line LNCaP

Evodiamine Induced Human Melanoma A375-S2 Cell Death Partially through Interleukin 1 Mediated Pathway

Evodiamine improves congnitive abilities in SAMP8 and APPswe/PS1ΔE9 transgenic mouse models of Alzheimer's disease

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