Tag: M.W=200-350

Lee, Stephanie M. published the artcileL-type calcium channels contribute to ethanol-induced aberrant tangential migration of primordial cortical GABAergic interneurons in the embryonic medial prefrontal cortex, COA of Formula: C17H18N2O6, the main research area is LTCC embryonic mPFC ethanol primordial cortical GIN tangential migration; FASD; GABA; alcohol; calcium; calcium channels; interneuron.

Exposure of the fetus to alc. (ethanol) via maternal consumption during pregnancy can result in fetal alc. spectrum disorders (FASD), hallmarked by long-term phys., behavioral, and intellectual abnormalities. In our preclin. mouse model of FASD, prenatal ethanol exposure disrupts tangential migration of corticopetal GABAergic interneurons (GINs) in the embryonic medial prefrontal cortex (mPFC). We postulated that ethanol perturbed the normal pattern of tangential migration via enhancing GABAA receptor-mediated membrane depolarization that prevails during embryonic development in GABAergic cortical interneurons. However, beyond this, our understanding of the underlying mechanisms is incomplete. Here, we tested the hypothesis that the ethanol-enhanced depolarization triggers downstream an increase in high-voltage-activated nifedipine-sensitive L-type calcium channel (LTCC) activity and provide evidence implicating calcium dynamics in the signaling scheme underlying the migration of embryonic GINs and its aberrance. Tangentially migrating Nkx2.1+ GINs expressed immunoreactivity to Cav1.2, the canonical neuronal isoform of the L-type calcium channel. Prenatal ethanol exposure did not alter its protein expression profile in the embryonic mPFC. However, exposing ethanol concomitantly with the LTCC blocker nifedipine prevented the ethanol-induced aberrant migration both in vitro and in vivo. In addition, whole-cell patch clamp recording of LTCCs in GINs migrating in embryonic mPFC slices revealed that acutely applied ethanol potentiated LTCC activity in migrating GINs. Based on evidence reported in the present study, we conclude that calcium is an important intracellular intermediary downstream of GABAA receptor-mediated depolarization in the mechanistic scheme of an ethanol-induced aberrant tangential migration of embryonic GABAergic cortical interneurons.

eNeuro published new progress about Body weight. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, COA of Formula: C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Viana-Mattioli, Sarah published the artcileSIRT1-dependent effects of resveratrol and grape juice in an in vitro model of preeclampsia, Synthetic Route of 21829-25-4, the main research area is preeclampsia resveratrol and grape juice sirtuin effect; Endothelium; Grape juice; Nitric oxide; Oxidative stress; Preeclampsia; Resveratrol; SIRT1.

Preeclampsia (PE) is a multifactorial hypertensive disorder of pregnancy that is partly responsible for both maternal and fetal morbidity and mortality levels worldwide. It has been recently discovered that sirtuin-1 (SIRT1) is reduced in the circulation and in an in vitro model of PE. Therefore, in this study, we investigated the effects of trans-resveratrol, a potent antioxidant and activator of SIRT1, on oxidative stress and nitric oxide (NO) production in an in vitro model of PE compared to gestational hypertensive (GH) and healthy pregnant (HP) women. Furthermore, we also evaluated the effects of an acute intake of grape juice on women with PE to assess whether it could mimic in vitro trans-resveratrol supplementation. (1) In the GH group, resveratrol decreased intracellular reactive oxygen species (ROS) and increased their antioxidant capacity, while inhibiting SIRT1 reestablished previous levels. (2) In PE, inhibition of SIRT1 increased antioxidant activity. (3) Intracellular NO and supernatant nitrite levels were increased by inhibiting SIRT1 in the PE group. (4) Grape juice intake increased intracellular NO levels vs. before grape juice intake control; however, the inhibition of SIRT1 before grape juice intake initially increased NO, but decreased it 1 h after grape juice intake. In conclusion, activating SIRT1 by using resveratrol alone may not be beneficial to women with PE, and GH and PE seem to have different responsive mechanisms to this mol. Furthermore, grape juice intake seems to have different effects compared to resveratrol supplementation alone in this in vitro model of PE, demonstrating the potential of the combination of other biol. active mols. from grape juice over the SIRT1-eNOS-NO in PE treatment.

Biomedicine & Pharmacotherapy published new progress about Antioxidants. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Synthetic Route of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Ferreira, Paula Benvindo published the artcileSupplementation with Spirulina platensis Prevents Uterine Diseases Related to Muscle Reactivity and Oxidative Stress in Rats Undergoing Strength Training, Category: pyridine-derivatives, the main research area is Spirulina supplementation muscle oxidative stress uterine disease; Spirulina platensis; muscle reactivity; oxidative stress; physical exercise; uterus.

Strength training increases systemic oxygen consumption, causing the excessive generation of reactive oxygen species, which in turn, provokes oxidative stress reactions and cellular processes that induce uterine contraction. The aim of this study was to evaluate the possible protective effect of Spirulina platensis (SP), an antioxidant blue algae, on the contractile and relaxation reactivity of rat uterus and the balance of oxidative stress/antioxidant defenses. Female Wistar rats were divided into sedentary (CG), trained (TG), and T + supplemented (TG50, TG100) groups. Reactivity was analyzed by AQCAD, oxidative stress was evaluated by the malondialdehyde (MDA) formation, and the antioxidant capacity was measured by the 2,2-diphenyl-1-picrylhydrazyl (DPPH) method. Strength training increased contractile reactivity and decreased the pharmaco-mech. component of relaxing reactivity in rat uterus. In addition, training decreased oxidation inhibition in the plasma and exercise increased oxidative stress in the uterine tissue; however, supplementation with algae prevented this effect and potentiated the increase in antioxidant capacity. Therefore, this study demonstrated that food supplementation prevents changes in reactivity and oxidative stress induced by strength training in a rat uterus, showing for the first time, that the uterus is a target for this exercise modality and antioxidant supplementation with S. platensis is an alternative means of preventing uterine dysfunction.

Nutrients published new progress about Antioxidants. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Category: pyridine-derivatives.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Suslu, Incilay published the artcileElectrochemical detection of antioxidant activities of 4-indolyl-5-oxo-6,6 (or 7,7) -dimethyl-1,4,5,6,7,8-hexahydroquinoline derivatives, Safety of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is hexahydroquinoline derivative nifedipine antioxidant activity differential pulse voltammetry.

Antioxidants used in different medical and industrial fields in order to prevent and delay oxidative stress. They play a crucial role in the protecting biol. systems against many diseases. 1,4-dihydropyridines are known as calcium channel modulators. Electrochem. techniques are simple, cheap and fast detection techniques and require small amounts of sample, so they offer advantages over commonly used anal. methods. Voltammetric methods have been applied to investigated the antioxidant activity of compounds in different fields. The proposed work is aimed at examining the electrochem. behavior of the 1,4-dihydropyridines by differential pulse voltammetry and hence the assessment of its antioxidant activity from the cathodic reduction peak of oxygen values. The peak current due to oxygen reduction was found to be proportional to the 1,4-dihydropyridines concentration of 0.1 – 0.5 mg/mL. The coefficient of antioxidant activity of 1,4-dihydropyridine derivatives were calculated and compared each other. Nifedipine used as a reference drug that is known as the calcium channel modulator and it is used to compare the antioxidant activities of 1,4-dihydropyridine-derived compounds

Journal of Research in Pharmacy published new progress about Antioxidants. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Safety of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Maher, M. A. published the artcileNifedipine alone or combined with sildenafil citrate for management of threatened preterm labour: a randomised trial, Category: pyridine-derivatives, the main research area is nifedipine sildenafil citrate human preterm labor; Nifedipine; prematurity; sildenafil citrate; threatened preterm labour; tocolytic therapy.

To study the tocolytic action of nifedipine combined with sildenafil citrate (SC) and if the combination is superior to nifedipine alone in inhibiting threatened preterm labour (PTL). Prospective randomised study. An Egyptian university hospital. Women with threatened PTL who received either nifedipine with SC or nifedipine alone. Patients were randomly allocated to receive either (1) nifedipine 20 mg orally (stat dose), followed by 10 mg orally every 6-8 h at the same time as vaginal administration of SC (25 mg at 8-hourly intervals) or (2) nifedipine alone. Medications were continued for 48-72 h. The percentage of women who remained undelivered during hospitalisation. From Jan. 2015 to Nov. 2016, 239 women were randomised. The baseline characteristics of participants were similar. Nifedipine combined with SC was associated with more women remaining undelivered (81.8 vs. 68.6%; P = 0.018) during hospitalisation. Regarding secondary outcomes, the addition of SC was also associated with fewer deliveries within 7 days of admission (9.1 vs. 20.3%; P = 0.014), prolonged latency (29 vs. 7 days; P = 0.002), fewer admissions to neonatal intensive care units (31.4 vs. 44.1%; P = 0.043), fewer very preterm deliveries (from 28 to <32 wk, 20.7 vs. 38.1%; P = 0.043), and increased neonatal birthweight (1900 vs. 1500 g; P = 0.018). Vaginal SC combined with nifedipine is an effective option for tocolytic therapy during threatened PTL. Vaginal SC enhances the tocolytic effect of nifedipine. BJOG published new progress about Birth weight. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Category: pyridine-derivatives.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Parker, John D. published the artcileComparison of short-acting versus extended-release nifedipine: Effects on hemodynamics and sympathetic activity in patients with stable coronary artery disease, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is coronary artery disease sympathetic activity hemodynamics nifedipine.

Abstract: We investigated the impact of short-acting and extended release nifedipine on sympathetic activity using radiotracer methodol. in patients with stable coronary artery disease in order to more accurately document the response of the sympathetic nervous system to different formulations of this dihydropyridine calcium channel antagonist. Participants were randomized to placebo, short-acting or extended release nifedipine for 7-10 days. On the final day, systemic blood pressure, cardiac filling pressures, cardiac output, plasma norepinephrine (NE) and total body NE spillover were measured at baseline (time 0) and repeated at intervals for 6 h. There were no differences in baseline measures between groups. Following the morning dose of study medication there were no changes in hemodynamics or sympathetic activity in the placebo group. However, there was a significant fall in blood pressure and a significant increase in total body NE spillover in both nifedipine groups. Importantly, the increase in sympathetic activity in response to short-acting nifedipine began earlier (30 min) and was much greater than that observed in the extended release group, which occurred later (270 min). These findings confirm that sustained therapy with nifedipine is associated with activation of the sympathetic nervous system which is dependent on the pharmacokinetics of the formulation.

Scientific Reports published new progress about Blood plasma. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Possomato-Vieira, Jose Sergio published the artcileCirculating levels of hydrogen sulphide negatively correlate to nitrite levels in gestational hypertensive and preeclamptic pregnant women, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is gestational hypertensive hydrogen sulfide neg correlate pregnant women; gestational hypertension; hydrogen sulphide; nitrite; preeclampsia; pregnancy.

Endothelial dysfunction is a hallmark of preeclampsia and the role of nitric oxide (NO) has been extensively studied in this pregnancy complication. In recent years, hydrogen sulfide (H2S) has arisen as a new gasotransmitter with an impact on endothelial function. However, the involvement of H2S in the pathophysiol. of preeclampsia is not fully understood, and only a few studies with limited sample size have investigated circulating levels of H2S in preeclamptic patients. Moreover, H2S levels have not been previously evaluated in gestational hypertension. Furthermore, the relationship between H2S and NO in these hypertensive disorders of pregnancy has yet to be determined We measured H2S levels in plasma of 120 healthy pregnant women, 88 gestational hypertensive and 62 preeclamptic women. We also measured plasma nitrite in a subset of patients and carried out correlation anal. between plasma H2S and nitrite in these three groups. We found that plasma H2S was elevated in preeclampsia and further increased in gestational hypertension compared to healthy pregnancy. Plasma nitrite was reduced in gestational hypertension and preeclampsia, and these levels were neg. correlated with H2S in both gestational hypertension and preeclampsia, but not in healthy pregnancy. Our results indicate that increases in H2S may represent a mechanism triggered as an attempt to compensate reduced NO in gestational hypertension and preeclampsia. Future studies are warranted to investigate the mechanisms underlying H2S/NO interaction on mediating endothelial dysfunction in these hypertensive disorders of pregnancy.

Clinical and Experimental Pharmacology and Physiology published new progress about Blood plasma. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Kim, BaRun published the artcileA differentiated Ca2+ signalling phenotype has minimal impact on myocardin expression in an automated differentiation assay using A7r5 cells, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is signalling phenotype myocardin expression vascular smooth muscle cell A7r5; Differentiation; High-content analysis; ImageJ; Microscopy; Smooth muscle.

Vascular smooth muscle cells are unusual in that differentiated, contractile cells possess the capacity to “”de-differentiate”” into a synthetic phenotype that is characterized by being replicative, secretory, and migratory. One aspect of this phenotypic modulation is a shift from voltage-gated Ca2+ signalling in elec. coupled, differentiated cells to increased dependence on store-operated Ca2+ entry and sarcoplasmic reticulum Ca2+ release in synthetic cells. Conversely, an increased voltage-gated Ca2+ entry is seen when proliferating A7r5 smooth muscle cells quiesce. We asked whether this change in Ca2+ signalling was linked to changes in the expression of the phenotype-regulating transcriptional co-activator myocardin or α-smooth muscle actin, using correlative epifluorescence Ca2+ imaging and immunocytochem. Cells were cultured in growth media (DMEM, 10% serum, 25 mM glucose) or differentiation media (DMEM, 1% serum, 5 mM glucose). Coinciding with growth arrest, A7r5 cells became elec. coupled, and spontaneous Ca2+ signalling showed increasing dependence on L-type voltage-gated Ca2+ channels that were blocked with nifedipine (5 μM). These synchronized oscillations were modulated by ryanodine receptors, based on their sensitivity to dantrolene (5 μM). Actively growing cultures had spontaneous Ca2+ transients that were insensitive to nifedipine and dantrolene but were blocked by inhibition of the sarco-endoplasmic reticulum ATPase with cyclopiazonic acid (10 μM). In cells treated with differentiation media, myocardin and αSMA immunoreactivity increased prior to changes in the Ca2+ signalling phenotype, while chronic inhibition of voltage-gated Ca2+ entry modestly increased immunoreactivity of myocardin. Stepwise regression analyzes suggested that changes in myocardin expression had a weak relationship with Ca2+ signalling synchronicity, but not frequency or amplitude. In conclusion, we report a 96-well assay and anal. pipeline to study the link between Ca2+ signalling and smooth muscle differentiation. This assay showed that changes in the expression of two mol. differentiation markers (myocardin and αSMA) tended to precede changes in the Ca2+ signalling phenotype.

Cell Calcium published new progress about Blood vessel. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Du, Congwu published the artcileCa2+ channel blockade reduces cocaine′s vasoconstriction and neurotoxicity in the prefrontal cortex, SDS of cas: 21829-25-4, the main research area is calicum channel blockade cocaine vasoconstriction neurotoxicity prefrontal cortex.

Cocaine profoundly affects both cerebral blood vessels and neuronal activity in the brain. The vasoconstrictive effects of cocaine, concurrently with its effects on neuronal [Ca2+]i accumulation are likely to jeopardize neuronal tissue that in the prefrontal cortex (PFC) could contribute to impaired self-regulation and compulsive cocaine consumption. Here we used optical imaging to study the cerebrovascular and neuronal effects of acute cocaine (1 mg/kg i.v.) and to examine whether selective blockade of L-type Ca2+ channels by Nifedipine (NIF) (0.5 mg/kg i.v.) would alleviate cocaine′s effects on hemodynamics (measured with cerebral blood volume, HbT), oxygenation (measured with oxygenated Hb, HbO2) and neuronal [Ca2+]i, which were concomitantly measured in the PFC of naive rats. Our results show that in the PFC acute cocaine significantly reduced flow delivery (HbT), increased neuronal [Ca2+]i accumulation and profoundly reduced tissue oxygenation (HbO2) and these effects were significantly attenuated by NIF pretreatment. They also show that cocaine-induced vasoconstriction is distinct from its increase of neuronal [Ca2+]i accumulation though both of them contribute to hypoxemia and both effects were attenuated by NIF. These results provide evidence that blockade of voltage-gated L-type Ca2+ channels might be beneficial in preventing vasoconstriction and neurotoxic effects of cocaine and give support for further clin. investigations to determine their value in reducing cocaine′s neurotoxicity in cocaine use disorders.

Translational Psychiatry published new progress about Blood volume. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, SDS of cas: 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Ravasenga, Tiziana published the artcileSpatial regulation of coordinated excitatory and inhibitory synaptic plasticity at dendritic synapses, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is synaptic plasticity dendritic synapses; GABA uncaging; GABAergic synaptic plasticity; calcium imaging; dendrites; gephyrin; glutamate uncaging; glutamatergic spines; glutamatergic synaptic plasticity; heterosynaptic plasticity; receptor lateral diffusion.

The induction of synaptic plasticity at an individual dendritic glutamatergic spine can affect neighboring spines. This local modulation generates dendritic plasticity microdomains believed to expand the neuronal computational capacity. Here, we investigate whether local modulation of plasticity can also occur between glutamatergic synapses and adjacent GABAergic synapses. We find that the induction of long-term potentiation at an individual glutamatergic spine causes the depression of nearby GABAergic inhibitory synapses (within 3 μm), whereas more distant ones are potentiated. Notably, L-type calcium channels and calpain are required for this plasticity spreading. Overall, our data support a model whereby input-specific glutamatergic postsynaptic potentiation induces a spatially regulated rearrangement of inhibitory synaptic strength in the surrounding area through short-range heterosynaptic interactions. Such local coordination of excitatory and inhibitory synaptic plasticity is expected to influence dendritic information processing and integration.

Cell Reports published new progress about Brain cortex. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem