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PubMed1993

Effect of TMB-8 on alpha-adrenoceptor agonist and KC1 induced-contractions in isolated rabbit aorta.

1. TMB-8 (10(-6) M-10(-4) M) depresses the contractile effect of the selective alpha 1-adrenoceptor agonists methoxamine and phenylephrine in the isolated rabbit aorta. 2. TMB-8 also depresses contractions evoked by 80 mM KCl in this tissue when used at similar concentrations. 3. The calcium antagonist nifedipine potentiates the inhibitory effect of TMB-8 on the alpha 1-contractions. 4. In preparations mounted in Ca-free solution containing 0.5 mM EGTA, 10(-4) M TMB-8 markedly depressed the contractions caused by both alpha 1-adrenoceptor agonists. 5. The Ca2+ agonist BAY K 8644 (10(-6) M) partially prevented the inhibitory effect of TMB-8 on 80 mM KCl contractions.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Extracellular calcium causes the release of calcium from intracellular stores in chick osteocytes.

We have recently demonstrated that a rise in the extracellular divalent cation concentration induces a rapid elevation of cytosolic calcium in chick osteocytes. Here, we demonstrate that cytosolic calcium elevation that occurs in osteocytes on exposure to elevated extracellular calcium is independent of membrane voltage and is insensitive to modulation by organic calcium channel modulators, namely, BAY K 8644, nicardipine, and nifedipine. However, the calcium elevation was sensitive to modulation by an intracellular calcium antagonist, TMB-8, suggesting that the cytosolic calcium elevation was due to mobilization of this cation from an intracellular store.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Thyrotropin-releasing hormone regulation of thyrotropin beta-subunit gene expression involves intracellular calcium and protein kinase C.

Our previous studies demonstrated TRH stimulation of TSH beta gene expression in rat pituitary cell cultures and GH3 tumor cells in a transient expression assay. To begin to characterize the gene-proximal elements of the pathways involved in TRH stimulation of TSH beta gene transcription, we examined the effects of factors that increase intracellular calcium concentration, [Ca2+]i, or activate protein kinase C on TSH beta promoter activity in transfected GH3 cells. TPA, a tumor-promoting phorbol ester, stimulated a dose-dependent increase in TSH beta promoter activity at 8 h similar to TRH (2-3-fold). TPA did stimulate protein kinase C activation without [Ca2+] mobilization. The calcium ionophore ionomycin increased cytoplasmic free [Ca2+] by stimulating both calcium influx and release from internal stores without affecting protein kinase C. Ionomycin also stimulated a dose-dependent increase (2-fold) in TSH beta promoter activity at 8 h. However, the voltage-dependent Ca2+ channel agonist Bay K 8644, which increased influx of extracellular calcium, had little or no effect on TSH beta gene expression until 48 h (5-fold). Similar effects on prolactin/mRNA levels were observed in these cells. Effects of these factors were not additive, suggesting a common pathway(s) to stimulate gene expression. Inhibition of intracellular calcium mobilization by treatment with 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate (TMB-8) inhibited ionomycin effects on gene expression without affecting phorbol ester activity, and, conversely, inhibition of protein kinase C activity by 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride (H-7) or TPA desensitization blocked TPA effects without affecting ionomycin activity.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

Calmodulin antagonists inhibit dihydropyridine calcium channel activator (BAY-K-8644) induced cGMP synthesis in pituitary tumor cells.

The dihydropyridine calcium channel activator, BAY-K-8644, stimulates cGMP formation in ACTH-secreting mouse AtT-20 clonal corticotrophs. The recent report that calmodulin antagonists could inhibit dihydropyridine binding in several tissues suggested that these agents might also affect the cyclic nucleotide response to BAY-K-8644. In fact, TMB-8, trifluoperazine, and melittin, described as in vitro antagonists of calmodulin-dependent enzyme activities, all inhibited BAY-K-8644 induced cGMP synthesis in a concentration-dependent manner. The antagonists had no effect on cGMP formation stimulated by sodium nitroprusside or sodium azide. The calcium channel antagonist, nifedipine, did not stimulate cGMP formation nor did it alter the effect of BAY-K-8644 on accumulation of the nucleotide; one explanation thus is that the cyclase involved in cGMP formation is coupled to a low affinity binding site for BAY-K-8644, which is less accessible to other dihydropyridines. The relation of cyclic GMP formation to the function of the calcium channel in AtT-20 cells remains unknown.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Induction of aneuploidy in Chinese hamster oocytes following in vivo treatments with trimethoxybenzoic compounds and their analogues.

Many inhibitors of tubulin polymerization have a trimethoxybenzene ring in their molecules. Such trimethoxybenzoic compounds and their analogues may therefore have a potency to induce meiotic nondisjunction of oocytes. In this study, a single dose of reserpine (0.5 microgram/g body weight), podophyllotoxin (20.0 micrograms/g b.w.), trimethoxybenzoic acid (500.0 micrograms/g b.w.) or vinblastine sulfate (3.0 micrograms/g b.w.) was injected intraperitoneally to mature female Chinese hamsters at the onset of the first meiotic spindle formation of oocytes. Within 6 h after spontaneous ovulation, MII oocytes were collected from the oviducts for morphological examination and cytogenetic analysis. The incidence of morphologically abnormal oocytes with unusually large first polar body or bodies increased significantly after the treatment with reserpine (18/202; 8.9%), podophyllotoxin (28/172; 16.3%) and vinblastine sulfate (63/197; 32.0%), as compared with the control (3/214; 1.4%). Chromosome analysis of oocytes revealed that podophyllotoxin and vinblastine sulfate were effective in inducing aneuploidy (62/154; 40.3% and 128/156; 82.1% vs. 3/198; 1.5% of the control) by inhibiting the formation of spindle microtubules at the first meiosis. Aneuploids were found more frequently in morphologically abnormal oocytes than in normal oocytes. No aneugenic activity of reserpine and trimethoxybenzoic acid was observed. These results indicate that trimethoxybenzoic compounds do not necessarily exhibit aneugenic activity.

Aneuploidy↗
PubMed2006

Tannic acid, a potent inhibitor of epidermal growth factor receptor tyrosine kinase.

Increasing evidence supports the hypothesis that tannic acid, a plant polyphenol, exerts anticarcinogenic activity in chemically induced cancers. In the present study, tannic acid was found to strongly inhibit tyrosine kinase activity of epidermal growth factor receptor (EGFr) in vitro (IC50 = 323 nM). In contrast, the inhibition by tannic acid of p60(c-src) tyrosine kinase (IC50 = 14 microM) and insulin receptor tyrosine kinase (IC50 = 5 microM) was much weaker. The inhibition of EGFr tyrosine kinase by tannic acid was competitive with respect to ATP and non-competitive with respect to peptide substrate. In cultured cells, growth factor-induced tyrosine phosphorylation of growth factor receptors, including EGFr, platelet-derived growth factor receptor, and basic fibroblast growth factor receptor, was inhibited by tannic acid. No inhibition of insulin-induced tyrosine phosphorylation of insulin receptor and insulin-receptor substrate-1 was observed. EGF-stimulated growth of HepG2 cells was inhibited in the presence of tannic acid. The inhibition of serine/threonine-specific protein kinases, including cAMP-dependent protein kinase, protein kinase C and mitogen-activated protein kinase, by tannic acid was only detected at relatively high concentration, IC50 being 3, 325 and 142 microM respectively. The molecular modeling study suggested that tannic acid could be docked into the ATP binding pockets of either EGFr or insulin receptor. These results demonstrate that tannic acid is an in vitro potent inhibitor of EGFr tyrosine kinase.

3T3 Cells↗
PubMed2006

Anti-Salmonella activity of constituents of Ardisia elliptica Thunb.

Antibacterial activity against veterinary Salmonella was determined using dried fruit extracts of Ardisia elliptica Thunb. Chromatographic purification and spectroscopic structure studies provided three active anti-Salmonella compounds, namely, syringic acid, isorhamnetin and quercetin. The minimal inhibitory concentrations (MICs) of the isolated compounds ranged between 15.6 and 125.0 microg mL(-1).

Anti-Bacterial Agents↗
PubMed1993

Rhythmic contractions of isolated small arteries from rat: role of calcium.

In order to investigate the mechanisms behind rhythmic contractions in small arteries of the mesenteric arcade from Wistar rats, the calcium dependency of the oscillations in response to noradrenaline activation was tested on isolated vessels. Application of 1 microM ryanodine or 30 microM TMB-8 (procedures known to inhibit Ca2+ release from intracellular stores) totally abolished the rhythmic activity, even though the antagonists had opposite effects on the amplitude of the contractile response to noradrenaline. Verapamil (1 microM) or felodipine (1 nM) (agents known to inhibit influx of extracellular Ca2+) also abolished the oscillations and reduced the maximal noradrenaline response by about 40%. Reducing the extracellular Ca2+ concentration to 0.1 mM reduced the amplitude of the noradrenaline response to a similar extent as 1 nM felodipine, but did not eliminate the oscillations. This may indicate that the effect of calcium entry blockers was to eliminate the voltage-dependency of Ca2+ inflow rather than just reducing the Ca2+ level. Manoeuvres that would increase the cytosolic Ca2+ concentration (exposure to caffeine or to the calcium agonist BAY-K 8644) increased the frequency of the oscillations. These observations indicate an important role, not only for voltage-operating channels, but also for intracellular calcium stores in the generation of rhythmic contractions in these small arteries. Oscillations appear to be generated by an interplay between membrane activation and intracellular calcium stores.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

Degradation of substituted mandelic acids by meta fission reactions.

A strain of Acinetobacter lwoffii degraded 4-hydroxymandelic and 4-hydroxy-3-methoxymandelic acids to their corresponding benzoates, which were then hydroxylated by specific monooxygenases to yield, respectively, protocatechuic and 3-O-methylgallic acids; these were substrates for meta fission dioxygenases. The product formed from 3-O-methylgallate underwent slow spontaneous cyclization at pH 7 to release methanol.

Acinetobacter↗
PubMed1985

Effects of TMB-8, an intracellular calcium antagonist, and W-7, a calmodulin antagonist, on prostaglandin output from the guinea-pig uterus.

TMB-8, an intracellular Ca2+ antagonist, inhibited the A23187-induced increase in outputs of prostaglandin (PG) F-2 alpha and 6-keto-PGF-1 alpha from the guinea-pig uterus superfused in vitro. The high basal output of PGF-2 alpha from the Day-15 guinea-pig uterus was not inhibited by TMB-8, indicating that a maintained high intracellular free Ca2+ concentration is not necessary for maintaining this high output of PGF-2 alpha. W-7, a calmodulin antagonist, had similar actions except that PGF-2 alpha output from the Day-15 uterus was reduced 20-30 min after the W-7 treatment had stopped. Overall, these findings suggest that, in the guinea-pig, oestradiol acting on a progesterone-primed uterus causes a prolonged stimulation of endometrial phospholipase A-2 in the absence of a maintained high Ca2+ concentration, thus providing a continuous release of arachidonic acid for increased endometrial PGF-2 alpha synthesis during the last third of the oestrous cycle.

6-Ketoprostaglandin F1 alpha↗
PubMed2002

[Studies on the chemical constituents from herba of Corallodiscus flabellata].

OBJECTIVE: To study the chemical constituents from Corallodiscus flabellata. METHOD: The compounds were isolated with macroporous adsorption resin, silica gel column chromatography and identified on the basis of their physiochemical and spectral data. RESULT: Six compounds were obtained and identified as vanillic acid, 3,4-dihydroxyphenylethyl-8-O-beta-D-glucopyranoside, syringic acid, caffeic acid, isoacteoside, ferulic acid. CONCLUSION: All the compounds were isolated from this plant for the first time.

Gallic Acid↗
PubMedDate not supplied

Induction of apoptosis by dopamine in human oral tumor cell lines.

Dopamine dose-dependently reduced the viable cell number of both human salivary gland tumor HSG and oral squamous cell carcinoma HSC-2, HSC-4, and NA cells. CoCl2 significantly reduced both the cytotoxic activity and radical intensity of dopamine (determined by ESR spectroscopy). Dopamine produced DNA fragments (demonstrated by TUNEL method) and induced degradation of cytokeratin by activated caspase in HSG cells (detected by an immunocytochemical method, using a specific M30 monoclonal antibody). FACS analysis demonstrated that dopamine induced DNA fragmentation, a biochemical hallmark of apoptosis, in human promyelocytic leukemia HL-60 cells. The addition of catalase did not prevent the apoptosis-inducing activity of dopamine, reducing the possibility of the involvement of H2O2 for dopamine-induced apoptosis. Dopamine transiently induced p38 mitogen-activated protein kinase (MAP kinase) phosphorylation. However, an inhibitor of p38 MAP kinase phosphorylation, SB203680, failed to inhibit the dopamine-induced apoptosis. These data suggest that p38 phosphorylation at an early stage may not be a causative event for apoptosis.

Apoptosis↗
PubMed2007

Hydrolyzable tannins with the hexahydroxydiphenoyl unit and the m-depsidic link: HPLC-DAD-MS identification and model synthesis.

This study was designed to develop efficient analytical tools for the difficult HPLC-DAD-MS identification of hydrolyzable tannins in natural tissue extracts. Throughout the study of the spectroscopic characteristics of properly synthesized stereodefined standards, it was observed that the UV-vis spectra of compounds with the m-depsidic link showed a characteristic shoulder at 300 nm, consistent with the simple glucogalloyl esters, whereas compounds with the hexahydroxydiphenoyl (HHDP) unit gave a diagnostic fragmentation pattern, caused by a spontaneous lactonization in the mass spectrometer. These observations were confirmed by HPLC-DAD-MS analyses of tannic acid and raspberry extracts, which are rich in hydrolyzable tannins with the m-depsidic link and the HHDP unit, respectively.

Chromatography, High Pressure Liquid↗
PubMed1996

Identification of an essential signaling cascade for mitogen-activated protein kinase activation by angiotensin II in cultured rat vascular smooth muscle cells. Possible requirement of Gq-mediated p21ras activation coupled to a Ca2+/calmodulin-sensitive tyrosine kinase.

In cultured rat vascular smooth muscle cells, angiotensin II (Ang II) induced a rapid increase in mitogen-activated protein kinase (MAPK) activity through the Ang II type 1 receptor, which was insensitive to pertussis toxin but was abolished by the phospholipase C inhibitor, U73122. The Ang II-induced MAPK activation was not affected by the protein kinase C inhibitor, GF109203X, and was only partially impaired by pretreatment with a phorbol ester, whereas both treatments completely prevented MAPK activation by the phorbol ester. Intracellular Ca2+ chelation by TMB-8, but not extracellular Ca2+ chelation or inhibition of Ca2+ influx, abolished Ang II-induced MAPK activation. The calmodulin inhibitor, calmidazolium, and the tyrosine kinase inhibitor, genistein, completely blocked MAPK activation by Ang II as well as by the Ca2+ ionophore A23187. Ang II caused a rapid increase in the binding of GTP to p21(ras), and this was inhibited by genistein, TMB-8, and calmidazolium but not by pertussis toxin or GF109203X. These data suggest that Ang II-induced MAPK activation through the Ang II type 1 receptor could be mediated by p21(ras)activation through a currently unidentified tyrosine kinase that lies downstream of Gq-coupled Ca2+/calmodulin signals.

Adenosine Triphosphate↗
PubMed1999

Mibefradil-induced inhibition of proliferation of human peripheral blood mononuclear cells.

To evaluate the role of intracellular calcium and particularly Ca2+-uptake in the initiation of lymphocyte mitogenesis, the effect of mibefradil, which blocks both L- and T-type calcium channels with a more selective blockade of T-type channels, on the proliferation of human peripheral blood mononuclear cells (PBMCs) is compared with the effect of nifedipine, which blocks only the L-type calcium channel. The rate of [3H]thymidine incorporation into control and concanavalin A-stimulated PBMCs in the presence or absence of the calcium channel blockers mibefradil or nifedipine (1, 10, or 50 microM), and of the intracellular calcium antagonist 3,4,5-trimethoxybenzoic acid 8-(diethylamino) octyl ester (TMB-8; 1, 10, 25, or 50 microM) was assayed in the cells cultured for 3 days. The cellular cytotoxicity and the cell number in growing cultures also was determined in mibefradil- or nifedipine-treated control or stimulated cells. Restoration of the proliferative response in mibefradil- or nifedipine-treated cells was investigated by addition of exogenous interleukin-2. Interleukin-2-receptor expression in the cells was monitored by using anti-activated T-cell antigen (Tac) antibody, and the interleukin-2 production in the cell supernatants of the cultures was determined by an enzyme-amplified sensitive immunoassay. Mibefradil and nifedipine concentration-dependently reduced the cell number and the [3H]thymidine incorporation or the de novo DNA synthesis in control and concanavalin A-stimulated human PBMCs. Mibefradil exhibited a more pronounced inhibition of the proliferation of human PBMCs than did nifedipine. The inhibitory effect of mibefradil or nifedipine on DNA synthesis was dependent on the timing of treatment with the drugs. The inhibitory effect of mibefradil or nifedipine on the lymphoproliferative response was nearly abolished if the drugs were added 20 h after cell stimulation. A markedly reduced inhibitory effect was found when mibefradil or nifedipine was added 1-7 h after cell stimulation. However, regardless of time of addition, TMB-8 caused a persistent inhibition of the proliferation of human PBMCs. The inhibitory effect of mibefradil or nifedipine on the proliferation of human PBMCs is nearly abolished by addition of the calcium channel activator Bay K 8644. The proliferative response of mibefradil- or nifedipine-treated cells is restored by addition of exogenous interleukin-2. The normal expression of interleukin-2 receptors was preserved, whereas the interleukin-2 production was blocked in the presence of mibefradil or nifedipine. Our data show that mibefradil has a more pronounced inhibitory effect on the proliferation of human PBMCs than nifedipine and that this inhibitory effect on DNA synthesis is dependent on the timing of treatment with both drugs.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2006

Real-time assay of immobilized tannase with a stopped-flow conductometric device.

A stopped-flow manifold was developed to assay and characterize immobilized tannase (EC 3.1.1.20). The immobilized enzyme reactor was inserted within the tube-type electrode pair (cell constant=103.2 cm(-1)) for a real-time conductometric measurement. Tris buffer (2 mM, pH=7.0) was used as the carrier for sensitivity improvement. The activities and kinetic parameters (Km values) for propyl gallate, methyl gallate and tannic acid were investigated.

Carboxylic Ester Hydrolases↗
PubMed1981

Bacterial degradation of 3,4,5-trimethoxycinnamic acid with production of methanol.

When grown on 3,4,5-trimethoxycinnamic acid, a strain of Pseudomonas putida oxidized this compound and also 3,4,5-trimethoxybenzoic, 3,5-dimethoxy-4-hydroxybenzoic (syringic), and 3,4-dihydroxy-5-methoxybenzoic (3-O-methylgallic) acids, but 3,5-dimethoxy-4-hydroxycinnamic and other acids bearing structural resemblances to the growth substrate were oxidized only slowly. These results indicate that two carbon atoms of the side chain of 3,4,5-trimethoxycinnamate were released before oxidative demethylation occurred to give the ring-fission substrate, 3-O-methylgallate. Oxidation of 3,4,5-trimethoxycinnamate by intact cells gave equimolar amounts of methanol, which was derived from the methoxyl group of 3-O-methylgallate. The tricarboxylic acids, 4-carboxy-2-keto-3-hexenedioic and 4-carboxy-4-hydroxy-2-ketoadipic acids, were shown to be formed by the action of a cell extract upon 3-O-methylgallate; therefore, methanol was released either during or immediately after fission of the benzene nucleus. Cell extracts, prepared from several independent soil isolates after growth on 3,4,5-trimethoxy derivatives of benzoic, cinnamic, and beta-phenylpropionic acids, rapidly oxidized 3-O-methylgallate without added cofactors. It is concluded that the reactions investigated serve generally as a source of methanol in nature.

Chemical Phenomena↗
PubMed2005

The predominant polyphenol in the leaves of the resurrection plant Myrothamnus flabellifolius, 3,4,5 tri-O-galloylquinic acid, protects membranes against desiccation and free radical-induced oxidation.

The predominant (>90%) low-molecular-mass polyphenol was isolated from the leaves of the resurrection plant Myrothamnus flabellifolius and identified to be 3,4,5 tri-O-galloylquinic acid using 1H and 13C one- and two-dimensional NMR spectroscopy. The structure was confirmed by mass spectrometric analysis. This compound was present at high concentrations, 44% (by weight) in hydrated leaves and 74% (by weight) in dehydrated leaves. Electron microscopy of leaf material fixed with glutaraldehyde and caffeine demonstrated that the polyphenols were localized in large vacuoles in both hydrated and dehydrated leaves. 3,4,5 Tri-O-galloylquinic acid was shown to stabilize an artificial membrane system, liposomes, against desiccation if the polyphenol concentration was between 1 and 2 microg/mug phospholipid. The phase transition of these liposomes observed at 46 degrees C was markedly diminished by the presence of 3,4,5 tri-O-galloylquinic acid, suggesting that the presence of the polyphenol maintained the membranes in the liquid crystalline phase at physiological temperatures. 3,4,5 Tri-O-galloylquinic acid was also shown to protect linoleic acid against free radical-induced oxidation.

Calorimetry, Differential Scanning↗