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Royal sun medicinal mushroom Agaricus brasiliensis (higher Basidiomycetes) and the attenuation of pulmonary inflammation induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).
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Agaricus brasiliensis currently is one of the most studied fungi because of its nutritional and therapeutic properties as an anti-inflammatory agent and an adjuvant in cancer chemotherapy. The effects of orally administered aqueous A. brasiliensis extract (14.3- and 42.9-mg doses) on parenchymal
Inhibitory effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on the metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in mouse lung explants.
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Our previous study showed that the nonsteroidal anti-inflammatory drug (NSAID), sulindac, inhibited lung tumorigenesis induced by the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). In this paper, we describe the metabolism of sulindac and its sulfide metabolite and
Modulation of Vascular Endothelial Growth Factor and Annexin A2 in Response to 4-(Methylnitrosamino)-1-(3-pyridyl)-1-Butanone -Induced Inflammation via Swimming Training.
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The nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK; nicotine derived nitrosamine ketone) is one of the strongest carcinogens in tobacco which is involved in induction of lung cancer by changing the stimulation of vascular endothelial growth factor (VEGF) and annexin A2 expression.
Recovery from 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced immunosuppression in A/J mice by treatment with nonsteroidal anti-inflammatory drugs.
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BACKGROUND
We have previously reported that nonsteroidal anti-inflammatory drugs inhibit lung tumorigenesis induced by the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in mice.
OBJECTIVE
The aims of this study were to determine if NNK suppresses humoral (i.e.,
Isolation of a new compound, 2-butanone 4-glucopyranoside 6'-O-gallate and other 8 compounds from the anti-inflammatory leave extracts of Memecylon edule Roxb.
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This present study was designed to isolate the compounds of Memecylon edule. The chemical compounds were purified by chromatographic methods and their structures were established on the basis of spectroscopic analyses (UV, MS and NMR). The major isolated compounds were tested for anti-inflammatory
Photobiological properties of nabumetone (4-[6-methoxy-2-naphthalenyl]-2-butanone), a novel non-steroidal anti-inflammatory and analgesic agent.
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The photolability of nabumetone (NB, 1, 4-[6-methoxy-2-naphthalenyl]-2-butanone) and its photobiological properties were studied under aerobic and anaerobic conditions using a variety of in vitro phototoxicity assays: photohemolysis, photoperoxidation of linoleic acid, and photosensitized
Toxicology and carcinogenesis studies of ozone and ozone 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone in Fischer-344/N rats.
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The purpose of this study was to evaluate the toxicity and potential carcinogenicity or cocarcinogenicity of ozone exposure in rats. Fischer-344/N (F-344/N) rats were exposed 6 hr/day, 5 days/wk, to 0, 0.12, 0.5, or 1.0 ppm ozone by inhalation for 2-yr and lifetime exposures. The cocarcinogenicity
4-(4-Hydroxy-3-methoxyphenyl)-2-butanone modulates redox signal in gamma-irradiation-induced nephrotoxicity in rats.
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Cellular exposure to ionising radiation leads to oxidative stress events, which refer to elevated intracellular levels of reactive oxygen species (ROS). The elevated levels of ROS significantly contributed to γ-radiation (IR) induced cytotoxicity. In an attempt to minimise these cytotoxic effects,
Cigarette toxin 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces experimental pancreatitis through α7 nicotinic acetylcholine receptors (nAChRs) in mice.
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Clinical studies have shown that cigarette smoking is a dose-dependent and independent risk factor for acute pancreatitis. Cigarette smoke contains nicotine which can be converted to the potent receptor ligand and toxin, NNK [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone]. Previously, we have shown
Combinations of indole-3-carbinol and silibinin suppress inflammation-driven mouse lung tumorigenesis by modulating critical cell cycle regulators.
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Chronic inflammation is an important risk factor for lung cancer. Therefore, identification of chemopreventive agents that suppress inflammation-driven lung cancer is indispensable. We studied the efficacy of combinations of indole-3-carbinol (I3C) and silibinin (Sil), 20 µmol/g diet each, against
RNA-sequencing studies identify genes differentially regulated during inflammation-driven lung tumorigenesis and targeted by chemopreventive agents.
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BACKGROUND
Chronic pulmonary inflammation has been consistently shown to increase the risk of lung cancer. Therefore, assessing the molecular links between the two diseases and identification of chemopreventive agents that inhibit inflammation-driven lung tumorigenesis is
Synthesis, antioxidant and anti-inflammatory activity of novel substituted ethylenediamines and ethanolamines. A preliminary quantitative structure-activity relationship study.
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Six substituted oxo- or hydroxy-aminoethanols and ethylenediamines were synthesized and tested as anti-inflammatory agents. 1-Substituted 4-(2-aminoethylamino)-1-butanones and 1-substituted 4-(2-hydroxy-ethylamino)-1-butanones were prepared by reacting the appropriate 4-chloro-1-butanone with the
BMS-229724 is a tight-binding inhibitor of cytosolic phospholipase A2 that acts at the lipid/water interface and possesses anti-inflammatory activity in skin inflammation models.
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Cytosolic phospholipase A2 (cPLA2) catalyzes the selective release of arachidonic acid from the sn-2 position of phospholipids and is believed to play a key cellular role in the generation of arachidonic acid. BMS-229724
Inhibition of COX-2 and induction of apoptosis: two determinants of nonsteroidal anti-inflammatory drugs' chemopreventive efficacies in mouse lung tumorigenesis.
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Recent studies suggested that nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit lung tumorigenesis under conditions that are immunosuppressive. We hypothesized that this inhibition of mouse lung tumorigenesis requires induction of apoptosis and inhibition of COX (cyclooxygenase)-1, COX-2, and
Effects of sulindac and oltipraz on the tumorigenicity of 4-(methylnitrosamino)1-(3-pyridyl)-1-butanone in A/J mouse lung.
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The efficacies of the non-steroidal, anti-inflammatory drug sulindac and the schistosomicidal agent oltipraz in inhibiting lung tumorigenesis was measured in A/J mice. Lung tumors (15.7 tumors/mouse) were induced by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
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