Compounds of four rings containing a nitrogen. They are biosynthesized from reticuline via rearrangement of scoulerine. They are similar to BENZYLISOQUINOLINES. Members include chelerythrine and sanguinarine.

Phosphatidylinositol 3-kinase and protein kinase C are required for the inhibition of caspase activity by epidermal growth factor. (1/443)

The mechanism by which growth factors exert an anti-apoptotic function on many cell types is not well understood. This issue is addressed in relation to epidermal growth factor (EGF) which inhibits apoptosis induced by staurosporine or wortmannin in an epithelial tumour cell line (CNE-2). The presence of EGF substantially reduced the in vitro Ac-DEVD-AMC hydrolytic activity and almost completely suppressed the intracellular cleavage of poly(ADP-ribose) polymerase in staurosporine- or wortmannin-treated cells. Staurosporine but not wortmannin caused the intracellular proteolytic processing of pro-caspase-3 and this event was transiently inhibited by EGF. Staurosporine-induced apoptosis was not inhibited by EGF in the presence of wortmannin or LY294002. Similarly, EGF failed to inhibit wortmannin-induced apoptosis in the presence of staurosporine, chelerythrine chloride or Go6850. These results suggest that phosphatidylinositol 3-kinase and protein kinase C play a role in the survival function of EGF but the reduction of cellular caspase activity cannot be satisfactorily explained by a lack of pro-caspase-3 activation.  (+info)

Effects of prostaglandin F2 alpha on intracellular pH, intracellular calcium, cell shortening and L-type calcium currents in rat myocytes. (2/443)

OBJECTIVE: We have studied the mechanisms underlying the positive inotropic action of prostaglandin F2 alpha (PGF2 alpha) by monitoring intracellular calcium transients, intracellular pH, L-type calcium currents and cell shortening in isolated ventricular myocytes. METHODS: Rat myocytes were loaded with fura-2AM for intracellular calcium measurements, or BCECF-AM for pH measurements. Cell shortening was recorded using an edge detection system, and L-type calcium currents measured using whole cell patch clamping. RESULTS: PGF2 alpha (3 nmol l-1-3 mumol l-1 increased single myocyte shortening and reduced resting cell length in a concentration-dependent manner. While myocyte shortening was increased by PGF2 alpha, this was not associated with any change in the amplitude of intracellular calcium transients, diastolic calcium, or L-type calcium currents. However, the same myocytes were capable of responding to catecholamines with increases in calcium transient amplitude and L-type calcium currents. PGF2 alpha (3 mumol l-1 caused a reversible rise in intracellular pH of 0.08 +/- 0.01 pH units (n = 5, p < 0.05). The Na(+)-H+ exchanger inhibitor, HOE 694 (10 mumol l-1, abolished the PGF2 alpha-induced rise in pH and the increase in cell shortening. PGF2 alpha-induced increases in cell shortening and intracellular pH were also attenuated by the protein kinase C (PKC) inhibitor, chelerythrine (2 mumol l-1. CONCLUSION: The positive inotropic action of PGF2 alpha appears to be mediated via activation of the Na(+)-H+ exchanger with the possible involvement of PKC. This suggests that PGF2 alpha-produces intracellular alkalosis, which then sensitizes cardiac myofilaments to calcium.  (+info)

Morphine preconditioning attenuates neutrophil activation in rat models of myocardial infarction. (3/443)

Previous results from our laboratory have suggested that morphine can attenuate neutrophil activation in patients with acute myocardial infarction. To elucidate if morphine preconditioning (PC) has the same effects via activation of neutrophil endopeptidase 24.11 (NEP), we measured serum levels of intercellular adhesion molecule-1 (ICAM-1), gp100MEL14 and NEP in adult Wistar rats subjected to ten different protocols (n = 10 for each) at baseline, immediately after and 2 h after morphine PC. All groups were subjected to 30 min of occlusion and 2 h of reperfusion. Similarly, morphine-induced PC was elicited by 3-min drug infusions (100 micrograms/kg) interspersed with 5-min drug-free periods before the prolonged 30-min occlusion. Infarct size (IS), as a percentage of the area at risk (AAR), was determined by triphenyltetrazolium staining. Pretreatment with morphine increased NEP activities (9.86 +/- 1.98 vs. 5.12 +/- 1.10 nmol/mg protein in control group; p < 0.001). Naloxone (mu-opioid receptor antagonist) (4.82 +/- 1.02 nmol/mg protein) and phosphoramidon (NEP inhibitor) (4.66 +/- 1.00 nmol/mg protein) inhibited morphine-activated NEP, whereas glibenclamide (ATP-sensitive potassium channel antagonist) and chelerythrine (protein kinase C inhibitor) had no effects. The ICAM-1 and gp100MEL14 of the third sampling were lowest for those with morphine PC (280 +/- 30 ng/ml and 2.2 +/- 0.7 micrograms/ml; p < 0.001), but naloxone (372 +/- 38 ng/ml and 3.8 +/- 0.9 micrograms/ml) and phosphoramidon (382 +/- 40 ng/ml and 4.2 +/- 1.1 micrograms/ml) abolished the above phenomenon. IS/AAR were definitely lowest for those with morphine PC (24 +/- 7%; p < 0.05). Morphine preconditioning increases NEP activities to attenuate shedding of gp100MEL14 and to ICAM-1 and, thus, provides myocardial protection.  (+info)

Isoform-selective activation of protein kinase C by nitric oxide in the heart of conscious rabbits: a signaling mechanism for both nitric oxide-induced and ischemia-induced preconditioning. (4/443)

Although isoform-selective translocation of protein kinase C (PKC) epsilon appears to play an important role in the late phase of ischemic preconditioning (PC), the mechanism(s) responsible for such translocation remains unclear. Furthermore, the signaling pathway that leads to the development of late PC after exogenous administration of NO in the absence of ischemia (NO donor-induced late PC) is unknown. In the present study we tested the hypothesis that NO activates PKC and that this is the mechanism for the development of both ischemia-induced and NO donor-induced late PC. A total of 95 chronically instrumented, conscious rabbits were used. In rabbits subjected to ischemic PC (six 4-minute occlusion/4-minute reperfusion cycles), administration of the NO synthase inhibitor Nomega-nitro-L-arginine (group III), at doses previously shown to block the development of late PC, completely blocked the ischemic PC-induced translocation of PKCepsilon but not of PKCeta, indicating that increased formation of NO is an essential mechanism whereby brief ischemia activates the epsilon isoform of PKC. Conversely, a translocation of PKCepsilon and -eta quantitatively similar to that induced by ischemic PC could be reproduced pharmacologically with the administration of 2 structurally unrelated NO donors, diethylenetriamine/NO (DETA/NO) and S-nitroso-N-acetylpenicillamine (SNAP), at doses previously shown to elicit a late PC effect. The particulate fraction of PKCepsilon increased from 35+/-2% of total in the control group (group I) to 60+/-1% after ischemic PC (group II) (P<0.05), to 54+/-2% after SNAP (group IV) (P<0.05) and to 52+/-2% after DETA/NO (group V) (P<0.05). The particulate fraction of PKCeta rose from 66+/-5% in the control group to 86+/-3% after ischemic PC (P<0.05), to 88+/-2% after SNAP (P<0.05) and to 85+/-1% after DETA/NO (P<0.05). Neither ischemic PC nor NO donors had any appreciable effect on the subcellular distribution of PKCalpha, -beta1, -beta2, -gamma, -delta, - micro, or -iota/lambda; on total PKC activity; or on the subcellular distribution of total PKC activity. Thus, the effects of SNAP and DETA/NO on PKC closely resembled those of ischemic PC. The DETA/NO-induced translocation of PKCepsilon (but not that of PKCeta) was completely prevented by the administration of the PKC inhibitor chelerythrine at a dose of 5 mg/kg (group VI) (particulate fraction of PKCepsilon, 38+/-4% of total, P<0.05 versus group V; particulate fraction of PKCeta, 79+/-2% of total). The same dose of chelerythrine completely prevented the DETA/NO-induced late PC effect against both myocardial stunning (groups VII through X) and myocardial infarction (groups XI through XV), indicating that NO donors induce late PC by activating PKC and that among the 10 isozymes of PKC expressed in the rabbit heart, the epsilon isotype is specifically involved in the development of this form of pharmacological PC. In all groups examined (groups I through VI), the changes in the subcellular distribution of PKCepsilon protein were associated with parallel changes in PKCepsilon isoform-selective activity, whereas total PKC activity was not significantly altered. Taken together, the results provide direct evidence that isoform-selective activation of PKCepsilon is a critical step in the signaling pathway whereby NO initiates the development of a late PC effect both after an ischemic stimulus (endogenous NO) and after treatment with NO-releasing agents (exogenous NO). To our knowledge, this is also the first report that NO can activate PKC in the heart. The finding that NO can promote isoform-specific activation of PKC identifies a new biological function of this radical and a new mechanism in the signaling cascade of ischemic PC and may also have important implications for other pathophysiological conditions in which NO is involved and for nitrate therapy.  (+info)

c-myc intron element-binding proteins are required for 1, 25-dihydroxyvitamin D3 regulation of c-myc during HL-60 cell differentiation and the involvement of HOXB4. (5/443)

1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) suppresses c-myc expression during differentiation of HL-60 cells along the monocytic pathway by blocking transcriptional elongation at the first exon/intron border of the c-myc gene. In the present study, the physiological relevance of three putative regulatory protein binding sites found within a 280-base pair region in intron 1 of the c-myc gene was explored. HL-60 promyelocytic leukemia cells were transiently transfected with three different c-myc promoter constructs cloned upstream of a chloramphenicol acetyltransferase (CAT) reporter gene. With the wild-type c-myc promoter construct (pMPCAT), which contains MIE1, MIE2, and MIE3 binding sites, 1,25-(OH)2D3 was able to decrease CAT activity by 45.4 +/- 7.9% (mean +/- S.E., n = 8). The ability of 1, 25-(OH)2D3 to inhibit CAT activity was significantly decreased to 18. 5 +/- 4.3% (59.3% reversal, p < 0.02) when examined with a MIE1 deletion construct (pMPCAT-MIE1). Moreover, 1,25-(OH)2D3 was completely ineffective at suppressing CAT activity in cells transfected with pMPCAT-287, a construct without MIE1, MIE2, and MIE3 binding sites (-6.5 +/- 10.9%, p < 0.002). MIE1- and MIE2-binding proteins induced by 1,25-(OH)2D3 had similar gel shift mobilities, while MIE3-binding proteins migrated differently. Furthermore, chelerythrine chloride, a selective protein kinase C (PKC) inhibitor, and a PKCbeta antisense oligonucleotide completely blocked the binding of nuclear proteins induced by 1,25-(OH)2D3 to MIE1, MIE2, and MIE3. A 1,25-(OH)2D3-inducible MIE1-binding protein was identified to be HOXB4. HOXB4 levels were significantly increased in response to 1,25-(OH)2D3. Taken together, these results indicate that HOXB4 is one of the nuclear phosphoproteins involved in c-myc transcription elongation block during HL-60 cell differentiation by 1,25-(OH)2D3.  (+info)

Importance of PKC and tyrosine kinase in single or multiple cycles of preconditioning in rat hearts. (6/443)

Both tyrosine kinase (TK) and protein kinase C (PKC) inhibitors have been shown individually to completely abolish the cardioprotective effects of ischemic preconditioning (IPC) in rabbits; however, blockade of both enzymes is necessary to totally abolish IPC in pigs. Recently, we have shown that TK inhibition partially attenuates the cardioprotective effect of IPC in intact rat hearts. Therefore, the present study was designed to test the hypothesis that inhibition of both TK and PKC is necessary to completely abolish IPC in the intact rat and that this effect is dependent on the intensity of the preconditioning stimulus. All animals were subjected to 30 min of coronary artery occlusion and 2 h of reperfusion. In series 1, multiple-cycle-induced IPC was produced via three 5-min occlusions interspersed with 5 min of reperfusion (3 x 5 IPC). Genistein (5 mg/kg), a TK inhibitor infused 30 min before IPC, and chelerythrine chloride (5 mg/kg), a PKC inhibitor infused 5 min before the prolonged ischemic insult, were administered alone or in combination in the absence or presence of 3 x 5 IPC. 3 x 5 IPC produced a marked reduction in infarct size as a percentage of area at risk compared with control (8.0 +/- 0.8 vs. 56.1 +/- 0.8%). The effects of 3 x 5 IPC were partially blocked by pretreatment with genistein (34.0 +/- 2.0%) or chelerythrine (26.4 +/- 2.8%) alone; however, combined administration of genistein and chelerythrine completely abolished the effects of 3 x 5 IPC (50.7 +/- 3.6%). In series 2, single-cycle IPC was elicited by one 5-min occlusion followed by 10 min of reperfusion (1 x 5 IPC). Compared with control, 1 x 5 IPC also significantly reduced infarct size (15.4 +/- 3.0%). Genistein or chelerythrine administered alone completely abolished 1 x 5 IPC-induced cardioprotection. These results suggest that the efficacy of TK and PKC inhibition to block IPC depends on the intensity of the preconditioning stimulus and that these kinases may work through parallel pathways.  (+info)

Chloride channel inhibition blocks the protection of ischemic preconditioning and hypo-osmotic stress in rabbit ventricular myocardium. (7/443)

The objective of this study was to examine the role of chloride (Cl-) channels in the myocardial protection of ischemic preconditioning (IP). Isolated rabbit ventricular myocytes were preconditioned with 10-minute simulated ischemia (SI) and 20-minute simulated reperfusion (SR) or not preconditioned (control). The myocytes then received 180-minute SI or 45-minute SI/120-minute SR. Indanyloxyacetic acid 94 (IAA-94, 10 micromol/L) or 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, 1 micromol/L) was administered before IP or before SI or SI/SR to inhibit Cl- channels. Electrophysiological studies indicate that these drugs, at the concentrations used, selectively abolished Cl- currents activated under hypo-osmotic conditions (215 versus 290 mOsm). IP significantly (P<0.001) reduced the percentage of dead myocytes after 60-minute (30.8+/-1.3%, mean+/-SEM), 90-minute (35.3+/-1.3%), and 120-minute (39.2+/-1.7%) SI compared with controls (44.7+/-1.6%, 54.5+/-1.3%, and 58.9+/-1.8%, respectively) and after 45-minute SI/120-minute SR (36.3+/-0.6%) compared with control (56.6+/-2.2%). Hypo-osmotic stress also produced protection similar to IP. IAA-94 or NPPB abolished the protection of both IP and hypo-osmotic stress. In buffer-perfused rabbit hearts preconditioned with three 5-minute ischemia/10-minute reperfusion cycles given before the 40-minute long ischemia and 60-minute reperfusion, IP significantly (P<0.0001) reduced infarct size (IP+vehicle, 4.7+/-0.9%, versus control+vehicle, 26.6+/-3.3%; mean+/-SEM). Again, IAA-94 or NPPB abolished the protection of IP. Our results implicate Cl- channels in the IP protection of the myocardium against ischemic/reperfusion injury and demonstrate that hypo-osmotic stress is capable of preconditioning cardiomyocytes.  (+info)

Nuclear factor-kappaB plays an essential role in the late phase of ischemic preconditioning in conscious rabbits. (8/443)

Although it is recognized that late preconditioning (PC) results from upregulation of cardioprotective genes, the specific transcription factor(s) that govern this genetic adaptation remains unknown. The aim of this study was to test the hypothesis that the development of late PC is mediated by nuclear factor-kappaB (NF-kappaB) and to elucidate the mechanisms that control the activation of NF-kappaB after an ischemic stimulus in vivo. A total of 152 chronically instrumented, conscious rabbits were used. A sequence of six 4-minute coronary occlusion/4-minute reperfusion cycles, which elicits late PC, induced rapid activation of NF-kappaB, as evidenced by a marked increase in p65 content (+164%; Western immunoblotting) and NF-kappaB DNA binding activity (+306%; electrophoretic mobility shift assay) in nuclear extracts isolated 30 minutes after the last reperfusion. These changes were attenuated 2 hours after ischemic PC and resolved by 4 hours. Competition and supershift assays confirmed the specificity of the NF-kappaB DNA complex signals. The mobility of the NF-kappaB DNA complex was shifted by anti-p65 and anti-p50 antibodies but not by anti-c-Rel antibodies, indicating that the subunits of NF-kappaB involved in gene activation after ischemic PC consist of p65-p50 heterodimers. Pretreatment with the NF-kappaB inhibitor diethyldithiocarbamate (DDTC; 150 mg/kg IP 15 minutes before ischemic PC) completely blocked the nuclear translocation and increased DNA binding activity of NF-kappaB. The same dose of DDTC completely blocked the cardioprotective effects of late PC against both myocardial stunning and myocardial infarction, indicating that NF-kappaB activation is essential for the development of this phenomenon in vivo. The ischemic PC-induced activation of NF-kappaB was also blocked by pretreatment with Nomega-nitro-L-arginine (L-NA), a nitric oxide synthase (NOS) inhibitor, N-2-mercaptopropionyl glycine (MPG), a reactive oxygen species (ROS) scavenger, chelerythrine, a protein kinase C (PKC) inhibitor, and lavendustin A, a tyrosine kinase inhibitor (all given at doses previously shown to block late PC), indicating that ischemic PC activates NF-kappaB via formation of NO and ROS and activation of PKC- and tyrosine kinase-dependent signaling pathways. A subcellular redistribution and increased DNA binding activity of NF-kappaB quantitatively similar to those induced by ischemic PC could be reproduced pharmacologically by giving the NO donor diethylenetriamine/NO (DETA/NO) (at a dose previously shown to elicit late PC), demonstrating that NO in itself can activate NF-kappaB in the heart. Taken together, these results provide direct evidence that activation of NF-kappaB is a critical step in the signal transduction pathway that underlies the development of the late phase of ischemic PC in conscious rabbits. The finding that four different pharmacological manipulations (L-NA, MPG, chelerythrine, and lavendustin A) produced similar inhibition of NF-kappaB suggests that this transcription factor is a common downstream pathway through which multiple signals elicited by ischemic stress (NO, ROS, PKC, tyrosine kinases) act to induce gene expression. To our knowledge, this is the first demonstration that NO can promote NF-kappaB activation in the heart, a finding that identifies a new biological function of NO and may have important implications for various pathophysiological conditions in which NO is involved and for nitrate therapy.  (+info)

Benzophenanthridines are a class of chemical compounds that contain a benzophenanthrene skeleton, which is a polycyclic aromatic hydrocarbon structure made up of three benzene rings fused together. Benzophenanthridine alkaloids are naturally occurring compounds found in plants and have various biological activities, including anti-inflammatory, antimicrobial, and antitumor properties. Some well-known benzophenanthridine alkaloids include sanguinarine, chelerythrine, and berberine. These compounds are known to interact with various biological targets such as enzymes, receptors, and DNA, making them of interest in pharmaceutical research and development.

The root contains benzophenanthridines and quinolines. Alkaloids: dictamnine. dimethylaheleryth-rine, austrosinensine, 8- ...
Dupont, C; Couillerot, E; Gillet, R; Caron, C; Zeches-Hanrot, M; Riou, JF; Trentesaux, C (2005). "The benzophenanthridine ... It also contains fagaronine, a benzophenanthridine alkaloid. A study by Williams, Soelberg and Jäger (2016) showed than ...
... is a benzophenanthridine alkaloid found in Zanthoxylum zanthoxyloides and other species in the genus Zanthoxylum. ... Dupont, C; Couillerot, E; Gillet, R; Caron, C; Zeches-Hanrot, M; Riou, JF; Trentesaux, C (2005). "The benzophenanthridine ...
This benzophenanthridine alkaloid can induce apoptosis in some transformed or malignant cell lines. D-Chelidonine, the main ... C. majus contains various isoquinoline alkaloids with protopine, protoberberine and benzophenanthridine structures. ...
... is a benzophenanthridine alkaloid present in the plant Chelidonium majus (greater celandine). It is a potent, ... "The actions of benzophenanthridine alkaloids, piperonyl butoxide and (S)-methoprene at the G-protein coupled cannabinoid CB₁ ...
Park SU, Yu M, Facchini PJ (2002). "Antisense RNA-mediated suppression of benzophenanthridine alkaloid biosynthesis in ... Dihydrobenzophenanthridine oxidase produces oxidized forms of benzophenanthridine alkaloids: In Sanguinaria canadensis ( ... cell suspensions and immobilized cultures for production of benzophenanthridine alkaloids". Appl. Microbiol. Biotechnol. 36 (5 ...
... the central enzyme in benzophenanthridine alkaloid biosynthesis". Phytochemistry. 29 (4): 1113-1122. doi:10.1016/0031-9422(90) ...
... is a benzophenanthridine alkaloid found in species of the genus Zanthoxylum , notably in Zanthoxylum nitidum. This ...
... an enzyme essential to the formation of benzophenanthridine alkaloids in the response of plants to pathogenic attack". Proc. ... a covalently flavinylated oxidase of benzophenanthridine alkaloid biosynthesis in plants". J. Biol. Chem. 270 (41): 24475-81. ...
... a covalently flavinylated oxidase of benzophenanthridine alkaloid biosynthesis in plants". The Journal of Biological Chemistry ...
Sanguinarine is a benzophenanthridine alkaloid (see phenanthridine), which, unlike most other alkaloids, has a red color in ...
Maiti, M.; G. S. Kumar (27 September 2007). "Molecular aspects on the interaction of protoberberine, benzophenanthridine, and ...
"The actions of benzophenanthridine alkaloids, piperonyl butoxide and (S)-methoprene at the G-protein coupled cannabinoid CB₁ ...
... benzophenanthridines, pyridophenanthridines, dibenzoquinolizines, terpenes, flavones, and furocoumarins. Tylophorine from ...
The benzophenanthridine alkaloid chelerythrine is the major active natural product found in Z. clava-herculis, exhibiting anti- ...
... versatile transformation has been used to generate polysubstituted lactam carboxylic acids and to prepare benzophenanthridine ...
The extract of bloodroot is called sanguinarine, a quaternary benzophenanthridine alkaloid which attacks and destroys living ...
Species identified in Nigeria contains several types of alkaloids including benzophenanthridines (nitidine, dihydronitidine, ...
A phenolic benzophenanthridine alkaloid from Fagara xanthoxyloides (1973) Torto, F.G.; Mensah, I.A. (April 1970). "Alkaloids of ... Comparative examination of two Zanthoxylum benzophenanthridine alkaloids for effects in rabbits (1989) Essential oils of Lippia ...
... benzophenanthridine, phthalide isoquinoline or rhoeadine metabolic pathways. Research on this matter is rare since it is very ...
They are derived from berberine, tetrahydroberberine, protopine and benzophenanthridine in Papaveroideae, and from ...
Effects of sodium orthovanadate on benzophenanthridine alkaloid formation and distribution in cell suspension cultures of ...
The root contains benzophenanthridines and quinolines. Alkaloids: dictamnine. dimethylaheleryth-rine, austrosinensine, 8- ...
Benzophenanthridine Alkaloids, BIOLOGICAL ACTIVITY, N-nucleophiles, nucleophilic addition, protoberberine alkaloids. Changed by ... protoberberine alkaloids;benzophenanthridine alkaloids; nucleophilic addition;N-nucleophiles; biological activity. Tags. ... Nucleophilic addition to protoberberine and benzophenanthridine skeleton. Authors. GRYCOVÁ, Lenka (203 Czech Republic), Dagmar ... KW - protoberberine alkaloids;benzophenanthridine alkaloids. KW - nucleophilic addition;N-nucleophiles. KW - biological ...
Chelerythrine is a benzophenanthridine alkaloid that is extracted from Chelidonium majus L., Macleaya cordata (Willd.) R. Br., ...
Krane, B.D., Fagbule, M.O., Shamma, M. and Gozler, B. (1984) The Benzophenanthridine Alkaloids. Journal of Natural Products, 47 ... cordata contain a variety of quaternary benzophenanthridine alkaloids (QBAs) that display multiple biological activities. ...
Plant sources of benzophenanthridine alkaloids and effects of these alkaloid on normal and cancer cells ... The content of the seven quaternary benzophenanthridine alkaloids (QBA) sanguinarine (SA), chelerythrine (CHE), chelirubine ( ...
In isolated, isometrically contracting left guinea pig atria, sanguinarine, a benzophenanthridine alkaloid from the papaveracea ...
7. The method of claim 6, wherein said biologically-active agent is selected from the group consisting of benzophenanthridine ... 8. The method of claim 5, wherein said biologically-active agent comprises a benzophenanthridine alkaloid. ... Sanguinarine chloride(SaCl), a benzophenanthridine alkaloid with antimicrobial activity especially toward periodontal pathogens ... and the benzophenanthridine alkaloids. To those skilled in the art, other drugs or biologically active agents that can be ...
Mass and nuclear magnetic resonance spectra of benzophenanthridine alkaloids. 1968, Vol. 33, Issue 5, pp. 1619-1623 [Abstract] ...
Benzophenanthridines - Preferred Concept UI. M0491452. Scope note. Compounds of four rings containing a nitrogen. They are ...
The interaction between a quaternary benzophenanthridine alkaloid chelerythrine (herein after, CHL) and bovine serum albumin ( ...
Benzophenanthridines. Berberine Alkaloids. Cell Line. Cell Line,Tumor. Cell Shape. Cell Survival. Cells. Comparative Study. Dna ... The benzophenanthridine alkaloids sanguinarine, chelerythrine and chelidonine were reported previously to provoke cell death in ...
A large number of Zanthoxylum species have been studied and most of them contain biologically active benzophenanthridine ...
It is we download fuel cell micro grids 2009; religion be what Benzophenanthridine; re theorizing for. Conversely doctoral can ... and DNase man especially Then as social benzophenanthridine and buckled books to regain Antiinflammatory academic prevention at ...
... which are accompanied by a small amount of N-methyllaurotetanine and the quaternary benzophenanthridines (sanguinarine, ...
This graph shows the total number of publications written about "Aporphines" by people in Harvard Catalyst Profiles by year, and whether "Aporphines" was a major or minor topic of these publication ...
The formation of benzophenanthridine alkaloids Higher-order cycloaddition reactions in natural product synthesis ...
Cytotoxic Benzophenanthridine and Benzylisoquinoline Alka-loids from Argemone mexicana. Z Naturforsch C J Biosci. 2003;58(7-8): ...
Patent 5133981: Purification of benzophenanthridine alkaloids extracts from alkaloid extracts. (ORGANIC COMPOUNDS -- PART OF ...
Speciation of Benzophenanthridine Alkaloids in Commercially Available Black Salve Products. Madison Harrier, Desirae Fledderman ...
Benzophenanthridine alkaloids (1). ... View More. Publication Date 2021 (3). 2019 (1). 2020 (1). 2022 (1). Has File(s) Yes (5) ... An update on the role of ROS in anticancer action of benzophenanthridine alkaloids Abdul Q., Khan; Rashid, Khalid; AlAmodi, ...
6-methoxydihydrosanguinarine (6-MS), a natural benzophenanthridine alkaloid extracted from Macleaya cordata (Willd.) R. Br, has ...
Quaternary benzophenanthridine alkaloid (QBA) and Protopine alkaloids (PA) extracted from Poppy. Several types of herb extract ... The recovery formula plus QBA+PA (quaternary benzophenanthridine alkaloid (QBA) and protopine alkaloids (PA)) that extracted ... The recovery formula plus QBA+PA (quaternary benzophenanthridine alkaloid (QBA) and protopine alkaloids (PA)) that extracted ...
Benzophenanthridines [D03.132.089] * Benzylisoquinolines [D03.132.098] * Betalains [D03.132.124] * Camptothecin [D03.132.151] ...
... and benzophenanthridine alkaloids [143]. BBE is a key rate-limiting enzyme in the synthesis of (S)-scoulerine. More recently, ... such as benzophenanthridine alkaloid sanguinarine (Table 1). It could interfere with Z-ring assembly through inhibiting ... a covalently flavinylated oxidase of benzophenanthridine alkaloid biosynthesis in plants. J. Biol. Chem. 1995, 270, 24475-24481 ...
1. Weiss, D., Baumert, A., Vogel, M. and Roos, W. Sanguinarine reductase, a key enzyme of benzophenanthridine detoxification. ...
Benzophenanthridines D3.494.633.207 D3.633.300.633.207 D3.549.131 D3.633.400.131 Benzophenones D2.455.426.559.389.115.124 ...
Benzophenanthridines D3.494.633.207 D3.633.300.633.207 D3.549.131 D3.633.400.131 Benzophenones D2.455.426.559.389.115.124 ...
Benzophenanthridines D3.494.633.207 D3.633.300.633.207 D3.549.131 D3.633.400.131 Benzophenones D2.455.426.559.389.115.124 ...
Benzophenanthridines D3.494.633.207 D3.633.300.633.207 D3.549.131 D3.633.400.131 Benzophenones D2.455.426.559.389.115.124 ...
  • Previous studies have shown that the aerial parts of M. cordata contain a variety of quaternary benzophenanthridine alkaloids (QBAs) that display multiple biological activities. (scirp.org)
  • The content of the seven quaternary benzophenanthridine alkaloids (QBA) sanguinarine (SA), chelerythrine (CHE), chelirubine (CHR), chelilutine (CHL), sanguilutine (SL), sanguirubine (SR) and macarpine (MA) was determined in the underground part of six plant species of the family Papaveraceae (Sanguinaria canadensis L., Dicranostigma lactucoides HOOK.f.et THOMS, Chelidonium majus L., Macleaya cordata (Willd. (muni.cz)
  • The benzophenanthridine alkaloids sanguinarine, chelerythrine and chelidonine were reported previously to provoke cell death in a variety of tumor cells suggesting their potential application as anticancer agents. (unideb.hu)
  • A large number of Zanthoxylum species have been studied and most of them contain biologically active benzophenanthridine alkaloids. (sanbi.org)
  • Eschscholtzine, allocryptopine, and protopine belong among the dominant tertiary alkaloids , which are accompanied by a small amount of N-methyllaurotetanine and the quaternary benzophenanthridines (sanguinarine, chelerythrine, chelirubine, chelilutine, and macarpine). (cas.cz)
  • The recovery formula plus QBA+PA (quaternary benzophenanthridine alkaloid (QBA) and protopine alkaloids (PA)) that extracted from Macleaya clordata (Poppy), It helps pain relief, inflammation relief and well responsive for treatment due to gastrointestinal hypomotility (ileus), bloat and colic. (randolphanimalhealthcare.com)
  • Most prickly ashes contain benzophenanthridine alkaloids, such as chelerythrine, and effective anti-microbial, and sanguinarine, and anti-inflammatory and dental plague inhibitor that also occurs in Sanguinaria canadensis ( See , Bloodroot ). (prcupcc.org)
  • Quaternary benzophenanthridine alkaloids are known to have a wide range of biological effects, including antimicrobial, antifungal, anti-inflammatory, and antitumour activities. (vfu.cz)
  • The aim of this study was to evaluate the anti-inflammatory potential of the five minor quaternary benzophenanthridine alkaloids sanguilutine, sanguirubine, chelirubine, chelilutine, and macarpine in vitro and to compare them with more thoroughly studied sanguinarine and chelerythrine. (vfu.cz)
  • The results obtained from the present experiments may provide additional information useful in understanding the structure-to-activity relationship of the quaternary benzophenanthridine alkaloids. (vfu.cz)
  • DNAbinding affinities and sequence selectivity of quaternary benzophenanthridine alkaloids sanguinarine, chelerythrine, and nitidine. (springer.com)
  • The benzophenanthridine alkaloids sanguinarine, chelerythrine and chelidonine were reported previously to provoke cell death in a variety of tumor cells suggesting their potential application as anticancer agents. (unideb.hu)
  • Benzophenanthridine alkaloids In The Alkaloids, Vol. 26, Brossi A. (ed. (idplink.net)
  • Inhibition of liver organ alanine aminotransferase activity by some benzophenanthridine alkaloids. (idplink.net)
  • Quaternary benzophenanthridine alkaloid (QBA) and Protopine alkaloids (PA) extracted from Poppy. (randolphanimalhealthcare.com)
  • Most prickly ashes contain benzophenanthridine alkaloids, such as chelerythrine, and effective anti-microbial, and sanguinarine, and anti-inflammatory and dental plague inhibitor that also occurs in Sanguinaria canadensis ( See , Bloodroot ). (prcupcc.org)
  • 6. The benzophenanthridine alkaloid fagaronine induces erythroleukemic cell differentiation by gene activation. (nih.gov)
  • DNA binding of benzophenanthridine compounds sanguinarine versus ethidium: Comparative binding and thermodynamic profile of intercalation. (springer.com)
  • Thermodynamic profiles of the DNA binding of benzophenanthridines sanguinarine and ethidium: A comparative study with sequence specific polynucleotides. (springer.com)