Uterotonic Effect of Evodia rutaecarpa Alkaloids

King, C. L.; Kong, Yao; Wong, Nikki Siu Hai; Yeung, H.W.; Fong, Harry H. S.; Sankawa, Ushio

doi:10.1021/np50011a008

Cited by 54 publications

(35 citation statements)

References 11 publications

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“…The role of EVO in the inhibition of tumor cell proliferation has been well-documented in a number of studies (13)(14)(15)(16)(17)(18)(19)(20), while our knowledge of the antitumor effects of EVO on OS cells remains rather sparse. To the best of our knowledge, this is the first study to explore whether EVO possesses anticancer activities in OS cells, and the possible molecular mechanism involved.…”

Section: Discussionmentioning

confidence: 99%

“…According to previous research, EVO was found to strongly inhibit tumor progression by reducing the proliferation rate and inducing apoptosis in a variety of tumor cells (13)(14)(15)(16)(17)(18)(19)(20). A series of analyses attempted to explain the underlying molecular mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…Evodiamine (EVO; 8,13,13b,14-tetrahydro-14-methylindolo [2'3'-3,4]pyrido [2,1-b]quinazolin-5-[7H]-one), a quinolone alkaloid isolated from a Chinese herbal medicinal plant Evodia rutaecarpa (10), plays multiple roles in biological physiological process, such as anti-inflammatory (11), anti-nociceptive (12) and uterotonic effects (13). Currently, evidence indicates that EVO possesses anticancer activities.…”

Section: Introductionmentioning

confidence: 99%

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Evodiamine inhibits the proliferation of human osteosarcoma cells by blocking PI3K/Akt signaling

Meng

Shu

et al. 2015

Oncology Reports

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Abstract. Osteosarcoma (OS) is the most common non-hematologic primary malignancy of bone, and multiple chemotherapeutic agents have been applied in the treatment of OS for over 40 years. Nevertheless, due to the poor prognosis of OS, it is essential to develop a novel treatment strategy. Evodiamine (EVO), a quinolone alkaloid extracted from the fruit of Evodia rutaecarpa, has been demonstrated to inhibit tumor cell proliferation. Thus, the main aim of the present study was to investigate the anti-proliferative and apoptosis-inducing effects of evodiamine (EVO) on human OS 143B cells, but also the possible mechanisms underlying these effects. The results of crystal violet staining, flow cytometry, western blot analysis and an in vivo experiment demonstrated that EVO exhibits significant inhibitory effects on cell proliferation, exhibits apoptosis-inducing effects and arrests the cell cycle in 143B cells. According to our findings of polymerase chain reaction (PCR), western blot analysis and recombinant adenoviral transfection, we confirmed that EVO upregulates both the protein and gene levels of phosphatase and tensin homolog (PTEN) in a concentration-dependent manner in 143B cells. Overexpression of PTEN reinforced the anti-proliferative effect of EVO in the 143B cells, while knockdown of PTEN upregulated PI3K/Akt signaling transduction and reversed the inhibitory effect of EVO on 143B cell proliferation. Further analysis indicated that EVO upregulated the expression of PTEN by inactivating PI3K/Akt signaling by decreasing phosphorylated Akt1/2. Based on the above results, we conclude that PTEN/PI3K/Akt signaling is involved in the inhibitory effect on human OS 143B cell proliferation by EVO.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Evodiamine inhibits the proliferation of human osteosarcoma cells by blocking PI3K/Akt signaling

Meng

Shu

et al. 2015

Oncology Reports

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“…We investigated whether rutaecarpine affects NF-B activation. The compound was isolated as previously described (59). KBM-5 cells were treated with rutaecarpine plus evodiamine and then with TNF.…”

Section: Evodiamine Represses Tnf-induced Nf-b-dependent Genementioning

confidence: 99%

Evodiamine Abolishes Constitutive and Inducible NF-κB Activation by Inhibiting IκBα Kinase Activation, Thereby Suppressing NF-κB-regulated Antiapoptotic and Metastatic Gene Expression, Up-regulating Apoptosis, and Inhibiting Invasion

Takada

Kobayashi

Aggarwal

2005

Journal of Biological Chemistry

171

102

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Evodiamine, an alkaloidal component extracted from the fruit of Evodiae fructus (Evodia rutaecarpa Benth., Rutaceae), exhibits antiproliferative, antimetastatic, and apoptotic activities through a poorly defined mechanism. Because several genes that regulate cellular proliferation, carcinogenesis, metastasis, and survival are regulated by nuclear factor-B (NF-B), we postulated that evodiamine mediates its activity by modulating NF-B activation. In the present study, we investigated the effect of evodiamine on NF-B and NF-B-regulated gene expression activated by various carcinogens. We demonstrate that evodiamine was a highly potent inhibitor of NF-B activation, and it abrogated both inducible and constitutive NF-B activation. The inhibition corresponded with the sequential suppression of IB␣ kinase activity, IB␣ phosphorylation, IB␣ degradation, p65 phosphorylation, p65 nuclear translocation, and p65 acetylation. Evodiamine also inhibited tumor necrosis factor (TNF)-induced Akt activation and its association with IKK. Suppression of Akt activation was specific, because it had no effect on JNK or p38 MAPK activation.

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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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Uterotonic Effect of Evodia rutaecarpa Alkaloids

Cited by 54 publications

References 11 publications

Evodiamine inhibits the proliferation of human osteosarcoma cells by blocking PI3K/Akt signaling

Evodiamine inhibits the proliferation of human osteosarcoma cells by blocking PI3K/Akt signaling

Evodiamine Abolishes Constitutive and Inducible NF-κB Activation by Inhibiting IκBα Kinase Activation, Thereby Suppressing NF-κB-regulated Antiapoptotic and Metastatic Gene Expression, Up-regulating Apoptosis, and Inhibiting Invasion

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

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