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aconitine/neoplasms

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Aconitine induces cell apoptosis in human pancreatic cancer via NF-κB signaling pathway.

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Pancreatic cancer is one of the leading causes of death from cancer in European countries and the United States. This study sought to investigate the effects of aconitine, a well-known aconitum plant-produced toxin, on pancreatic cancer cell growth and apoptosis and to explore the potential

Aconitine inhibits the proliferation of hepatocellular carcinoma by inducing apoptosis.

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Hepatocellular carcinoma (HCC) is the primary liver cancer that occurs with a high incidence in Asia. Owing to the poor prognosis of the disease, the mortality rate remains high, making HCC the third most common cause of cancer-related mortality worldwide. Studies on current therapies have generated

In vitro and in vivo anticancer activity of aconitine on melanoma cell line B16.

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The anti-tumor effect of aconitine in melanoma cell line B16 has been studied in this paper. We found that B16 cells showed significantly reduced growth rates and increased apoptotic effects in the presence of aconitine. Furthermore, aconitine inhibited the PI3K/AKT and MAPK/ERK1/2 signaling

Anticancer activity of aconitine-containing herbal extract BC1.

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OBJECTIVE The objective of the study was the investigation of anticancer activity of aconitine-containing herbal extract BC1 against two tumor strains with different metastatic potency: strongly metastatic Lewis lung carcinoma (LLC) and its weakly metastatic counterpart (LLC-R9). RESULTS It was

Aconitine-containing agent enhances antitumor activity of dichloroacetate against Ehrlich carcinoma.

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Significant variability of anticancer efficacy of dichloroacetate (DCA) stimulated an active search for the agents capable to enhance it antitumor action. Therefore, the aim of this work is the study of capability of aconitine-containing antiangiogenic agent BC1 to enhance anticancer activity of DCA

Cancer inhibition mechanism of lung cancer mouse model based on dye trace method.

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To minimize the incidence and mortality of cancer, dye trace method was used to explore the mechanism of drug inhibition. 60 mice were selected as the research objects and randomly divided into five groups: model group, shikonin group, aconitine group, notoginsenoside R1 group, and compound group.

The exposure of highly toxic aconitine does not significantly impact the activity and expression of cytochrome P450 3A in rats determined by a novel ultra performance liquid chromatography-tandem mass spectrometric method of a specific probe buspirone.

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Aconitum species are widely used to treat rheumatism, cardiovascular diseases, and tumors in China and other Asian countries. The herbs are always used with drugs such as paclitaxel. Aconitine (AC) is one of the main bioactive/high-toxic alkaloids of Aconitum roots. AC is metabolized by cytochrome

The influences of aconitine, an active/toxic alkaloid from aconitum, on the oral pharmacokinetics of CYP3A probe drug buspirone in rats.

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Aconitine (AC), an active/toxic alkaloid from Aconitum species, is commonly present in Traditional Chinese Medicine (TCM) prescriptions because of the great effectiveness of Aconitum for the treatment of rheumatoid arthritis, cardiovascular diseases, and tumors in clinic. Buspirone (BP) is a

The role of efflux transporters on the transport of highly toxic aconitine, mesaconitine, hypaconitine, and their hydrolysates, as determined in cultured Caco-2 and transfected MDCKII cells.

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Aconitum alkaloids including aconitine (AC), mesaconitine (MA), hypaconitine (HA), are highly toxic. Their hydrolysates, such as benzoylaconine (BAC), benzoylmesaconine (BMA), benzoylhypaconine (BHA), aconine, and mesaconine, are considerably less toxic. Efflux transporters, including P-glycoprotein

Antioxidant and antiproliferative effects of different solvent fractions from Terminalia belerica Roxb. fruit on various cancer cells.

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Terminalia belerica Roxb. fruits have been previously reported against diabetes, ulcer, microbial problems and hepatotoxicity. The present study was aimed to investigate antioxidant and anticancer potential of sequentially fractionated hexane (TBHE), chloroform (TBCE), ethyl acetate (TBEE), butanol

Antitumor effects of aconitine in A2780 cells via estrogen receptor β‑mediated apoptosis, DNA damage and migration

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Ovarian cancer (OVCA) is the deadliest type of malignant gynecological disease, and previous studies have demonstrated that estrogen receptor β (ERβ) serves important roles in this disease. Aconitine, a toxin produced by the Aconitum plant, displays potent effects against cancers. The aim of the

Cytotoxic Effects of Diterpenoid Alkaloids Against Human Cancer Cells.

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Diterpenoid alkaloids are isolated from plants of the genera Aconitum, Delphinium, and Garrya (Ranunculaceae) and classified according to their chemical structures as C18-, C19- or C20-diterpenoid alkaloids. The extreme toxicity of certain

Aconitum alkaloids, the major components of Aconitum species, affect expression of multidrug resistance-associated protein 2 and breast cancer resistance protein by activating the Nrf2-mediated signalling pathway.

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BACKGROUND Aconitum alkaloids from Aconitum species are often used to treat arthritis and rheumatic diseases but have the drawback of high toxicity. Identifying their pharmacokinetic behaviour is important for the safe clinical application of Aconitum species. Efflux transporters (ETs), including

Influence of aconitine-containing herbal extract BC1 on proliferative and electrokinetic characteristics of endothelial cells.

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OBJECTIVE To evaluate the influence of new antitumor preparation BC1 produced on the base of Aconitum species on viability and electrokinetic properties of endothelial cells for estimation of mechanisms of its antitumor and antimetastatic activity. METHODS Cytotoxic/cytostatic action of BC1 toward

Aconitum-Derived Bulleyaconitine A Exhibits Antihypersensitivity Through Direct Stimulating Dynorphin A Expression in Spinal Microglia.

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Aconitine and its structurally-related diterpenoid alkaloids have been shown to interact differentially with neuronal voltage-dependent sodium channels, which was suggested to be responsible for their analgesia and toxicity. Bulleyaconitine A (BAA) is an aconitine analogue and has been prescribed
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