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The Potential of Plants as Treatments for Venous Thromboembolism
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Lilitha L. Denga, Namrita Lall
Coumarin derivatives have attractive anticoagulant Vitamin K antagonist activity (Lei et al. 2015). Dicoumarol is a Vitamin K antagonist produced by fungal species such as Penicillium nigricans and Penicillium jensi on Melilotus alba Medik. and Melilotus officinalis (L.) Pall. (sweet clover) (Madari et al. 2003). Dicoumarol is the building block for modern-day Vitamin K antagonists, and its derivatives are hydroxylated in position 4 and have a substitution in position 3 (Lei et al. 2015). These are the minimum requirements for the anticoagulant activity of coumarins. Warfarin is a synthetic derivative of dicoumarol synthesized by the Michael addition of 4-hydroxycoumarin and benzolactone (Jain and Joshi 2012).
Phenobarbital
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
PB is a potent inducing agent for many enzyme systems, both hepatic and extrahepatic. Consequently, it may accelerate the rate of metabolism of other drugs and endogenous compounds. A list of potentially clinically significant interactions in which PB may increase the clearance of other drugs is presented in Table 2. Other drugs may increase the serum concentrations of PB. Such an effect has been reported for dicoumarol (9), frusemide (10), methylphenidate (11), propoxyphene (12), and VPA (13). The interaction with VPA is striking and has led to barbiturate-induced coma.
The twentieth century
Published in Michael J. O’Dowd, The History of Medications for Women, 2020
Heparin was found to be an antithrombin, an antiprothrombin, and an antithromboplastin, and proved to be the most important, the safest, and the most certain of the anticoagulant drugs. A ready antidote existed in the form of a 1% solution of protamine sulfate. Unlike the dicumarol type of anticoagulants, the heparin molecule was too large to cross the placenta and was safe to use in pregnancy. The use of heparin in vitro to prevent blood from clotting led to its use to prevent venous thrombosis.
Advances in determining new treatments for hepatitis B infection by utilizing existing and novel biomarkers
Published in Expert Opinion on Drug Discovery, 2023
Lung-Yi Mak, Rex Wan-Hin Hui, Ka-Shing Cheung, James Fung, Wai-Kay Seto, Man-Fung Yuen
Some more classes of agents are currently being evaluated in the pre-clinical phase. Dihydroquinolizinone compounds (e.g. RG7834) are an orally available small molecule that binds to host proteins PAPD5/7 and destabilize HBV mRNA[96]. Drugs that target the cccDNA adopt either a gene editing or non-gene editing approach. For gene editing approach, nucleases can be designed to cleave a specific DNA sequence, e.g. in the S gene or episomal cccDNA, and lead to gene disruption and eventually inactivation of the gene. These include zinc finger proteins, transcription activator-like effector nucleases, clustered regularly interspaced short palindromic repeats (CRISPR) with CRISPR-associated 9 (Cas9), and homing endonucleases [97–103]. In the non-gene editing approach, the APOBEC3B pathway can be amplified and give rise to similar effects as PEG-IFNα [38]. The cccDNA destabilization can also be achieved via alternative pathways (e.g. ccc_R08). HBx is a potential target as it is heavily involved in regulating cccDNA transcription. HBx destroys a host of restrictive structural maintenance of chromosome (SMC) complex that is responsible for inhibition of viral transcription [104,105]. The NEDD8-activating enzyme (NAE) responsible for degrading SMC5/6 can be inhibited (e.g. Pevonedistat) and restore SMC5/6 function. [106] HBx can also be destabilized by NAPDH quinone oxidoreductase (NQO1) inhibitor (e.g. Dicoumarol). [107]
Chemoprevention of Prostate Cancer Cells by Vitamin C plus Quercetin: role of Nrf2 in Inducing Oxidative Stress
Published in Nutrition and Cancer, 2021
Ali Abbasi, Zohreh Mostafavi-Pour, Ahmad Amiri, Fatemeh Keshavarzi, Negar Nejabat, Fatemeh Ramezani, Ahmadreza Sardarian, Fatemeh Zal
After culturing the cells (12 × 105) in T75 flask and sequential treating with different doses (100 or 200 µM) of VC for 24 h and following by different doses (50 or 75 µM) of Q for 6 h, 2 ml 25 mM Tris-HCl buffer (pH = 7.4) and 250 mM sucrose (1:1) were added to the cells and the cells were lysed using sonicator (For four times, 10 s each time on ice). After this step, the cell lysates were centrifuged at 10,000 × g for 30 s at 4 °C and enzyme activity was measured in the supernatant of cell lysates. NADH is oxidized as an electron donor and dichloroindophenol (DCPIP) as the electron acceptor is reduced in the presence of the NQO1 enzyme, which is associated with the loss of DCPIP color, and the investigation of these color changes is used to landslide the enzyme activity. The method and amount of materials used to measure enzyme activity were similar to a previous study performed by the authors (30). Dicoumarol was used as inhibitor and terminator of the reaction. NQO1 final activity was defined as nM/min/mg protein.
Metabolic characteristics of Tanshinone I in human liver microsomes and S9 subcellular fractions
Published in Xenobiotica, 2019
Yue Li, Yujuan Fan, Huizong Su, Qian Wang, Guo-Fu Li, Yiyang Hu, Jian Jiang, Bo Tan, Furong Qiu
Inhibition studies were conducted in the HLMs and S9 fractions with reductase inhibitors. Chlorpromazine (100 μM; AOX), allopurinol (100 μM; XOR), emodin (10 μM; 11β-HSD1), 2-CEE (10 mM; NADPH-P450 reductase) and dicoumarol (50 μM; NQO1) were selected as respective inhibitors as literatures (Barr & Jones, 2011; Diamond et al., 2010; Feng et al., 2010; Wu et al., 2017). The five enzymes have different subcellular distributions. AOX and XOR exist in cytosol, while 11β-HSD1 and NADPH-P450 reductase exist in microsomes. The majority of NQO1 exist in cytosol, but a few exist in microsomes and mitochondria (Danielson et al., 1960). Hence, S9 fractions were used for AOX and XOR inhibition studies, and HLMs were employed for 11β-HSD1 and NADPH-P450 reductase test. NQO1 inhibition was tested in both S9 fractions and HLMs. The incubation mixture contained 0.2 mg/mL HLMs or S9 fractions, 50 μg/mg alamethicin, inhibitors at corresponding concentrations, 5 mM MgCl2, 0.1 M potassium phosphate buffer (pH 7.4), 2 µM TSI, 1 mM NADPH and 2 mM UDPGA. Control samples were prepared without reductase inhibitors.