Tag: 100-200

Vegas-Suarez, Sergio;Aristieta, Asier;Requejo, Catalina;Bengoetxea, Harkaitz;Lafuente, Jose Vicente;Miguelez, Cristina;Ugedo, Luisa published 《The effect of 5-HT_1A receptor agonists on the entopeduncular nucleus is modified in 6-hydroxydopamine-lesioned rats》. The research results were published in《British Journal of Pharmacology》 in 2021.Recommanded Product: N,2-Dihydroxybenzamide The article conveys some information:

L-DOPA prolonged treatment leads to disabling motor complications as dyskinesia that could be decreased by drugs acting on 5-HT1A receptors. Since the internal segment of the globus pallidus, homologous to the entopeduncular nucleus in rodents, seems to be involved in the etiopathol. of L-DOPA-induced dyskinesia, we investigated whether the entopeduncular nucleus is modulated by the 5-HT_1A receptor partial and full agonists, buspirone, and 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT) in control and 6-hydroxydopamine (6-OHDA)-lesioned rats with or without long-term L-DOPA treatment. Extracellular single-unit electrocorticogram and local field potential recordings under anesthesia, immunostaining assays and optogenetic manipulation coupled to electrophysiol. recordings were performed. Systemic buspirone reduced the entopeduncular nucleus firing rate in the sham animals and burst activity in the 6-OHDA-lesioned rats (with or without L-DOPA treatment), while local administration reduced entopeduncular nucleus activity in all the groups, regardless of DA integrity. Systemic 8-OH-DPAT also induced inhibitory effects only in the sham animals. Effects triggered by buspirone and 8-OH-DPAT were reversed by the 5-HT_1A receptor antagonist, WAY-100635. Neither buspirone nor 8-OH-DPAT modified the low-frequency oscillatory activity in the entopeduncular nucleus or its synchronization with the motor cortex. Buspirone did not alter the response induced by subthalamic nucleus opto-stimulation in the entopeduncular nucleus. Systemic 5-HT_1A receptor activation elicits different effects on the electrophysiol. properties of the entopeduncular nucleus depending on the integrity of the nigrostriatal pathway and it does not alter the relationship between subthalamic nucleus and entopeduncular nucleus neuron activity. To complete the study, the researchers used N,2-Dihydroxybenzamide (cas: 89-73-6) .

N,2-Dihydroxybenzamide(cas: 89-73-6) is a hydroxamic acid that inhibits the activity of p-hydroxybenzoic acid (PHBA) reductase, an enzyme involved in the conversion of PHBA to benzoic acid. Recommanded Product: N,2-Dihydroxybenzamide The compound has been shown to inhibit mitochondrial membrane potential and mitochondrial functions, leading to cell death.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Vega de Luna, Felix;Cordoba-Granados, Juan Jose;Dang, Kieu-Van;Roberty, Stephane;Cardol, Pierre published 《In vivo assessment of mitochondrial respiratory alternative oxidase activity and cyclic electron flow around photosystem I on small coral fragments》 in 2020. The article was appeared in 《Scientific Reports》. They have made some progress in their research.Name: N,2-Dihydroxybenzamide The article mentions the following:

The mutualistic relationship existing between scleractinian corals and their photosynthetic endosymbionts involves a complex integration of the metabolic pathways within the holobiont. Respiration and photosynthesis are the most important of these processes and although they have been extensively studied, our understanding of their interactions and regulatory mechanisms is still limited. In this work we performed chlorophyll-a fluorescence, oxygen exchange and time-resolved absorption spectroscopy measurements on small and thin fragments (0.3 cm2) of the coral Stylophora pistillata. We showed that the capacity of mitochondrial alternative oxidase accounted for ca. 25% of total coral respiration, and that the high-light dependent oxygen uptake, commonly present in isolated Symbiodiniaceae, was negligible. The ratio between photosystem I (PSI) and photosystem II (PSII) active centers as well as their resp. electron transport rates, indicated that PSI cyclic electron flow occurred in high light in S. pistillata and in some branching and lamellar coral species freshly collected in the field. Altogether, these results show the potential of applying advanced biophys. and spectroscopic methods on small coral fragments to understand the complex mechanisms of coral photosynthesis and respiration and their responses to environmental changes. The experimental procedure involved many compounds, such as N,2-Dihydroxybenzamide (cas: 89-73-6) .

N,2-Dihydroxybenzamide(cas: 89-73-6) is widely used for a variety of roles in biology and medicine as a chelating therapy.Name: N,2-DihydroxybenzamideIt inhibits bacterial or fungi growth by interfering with iron uptake. It is also active as a inhibitor of enzyme involved in tumour growths.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Chuan, Libo;Huang, Xin;Fan, Chuming;Wen, Shiyuan;Yang, Xiaohua;Wang, Jingrong;Ren, Jingyu;Ru, Jin;Ding, Li published 《Metformin ameliorates brain damage caused by cardiopulmonary resuscitation via targeting endoplasmic reticulum stress-related proteins GRP78 and XBP1》. The research results were published in《European Journal of Pharmacology》 in 2021.Synthetic Route of C7H7NO3 The article conveys some information:

Cerebral damage after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) is a primary cause of death. Endoplasmic reticulum stress (ERS) is very important during these situations. This study aimed to explore the role of metformin in protecting brain endoplasmic reticulum post CA/CPR. Male SD rats (n = 132) were treated with 6-min CA-posted asphyxia and sham surgery. Before CA/CPR, metformin (200 mg/kg/day) or a vehicle (0.9% saline) were administered randomly for two weeks. The neurol. deficit scores were assessed 24 h, 48 h, 72 h, and 7 days after CA/CPR, and the rat brains were analyzed by Western blotting and qRT-PCR. Apoptosis was detected by the TUNEL assay according to the mitochondrial membrane potential (MMP). Oxidative stress and ERS-related protein expression were also investigated. The Western blotting and qRT-PCR results revealed that the resuscitated animals had time-dependent elevated GRP78 and XBP1 levels compared with the sham operative rats. Moreover, our results showed that the rats treated with metformin had increased neurol. deficit scores (NDS), an improved seven-day survival rate, decreased cell apoptosis within the hippocampus CA1 area, and less oxidative stress compared with the CA/CPR group. Furthermore, metformin inhibited the mRNA and protein expressions of glucose-regulated protein 78 (GRP78) and X-box binding protein 1 (XBP1) in the CA/CPR rat model. We confirmed that CA/CPR can induce ERS-related apoptosis and oxidative stress in the brain; moreover, inhibiting ERS-related proteins GRP78 and XBP1 with metformin might attenuate cerebral injury post CA/CPR. To complete the study, the researchers used N,2-Dihydroxybenzamide (cas: 89-73-6) .

N,2-Dihydroxybenzamide(cas: 89-73-6) can be used:To prepare phenylboronic acid-based bioconjugates for chromatographic applications;As a ligand to synthesize Fe(III), Cu(II), Ni(II) and Zn(II) complexes.Synthetic Route of C7H7NO3

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Quality Control of 6-AminonicotinamideIn 2016, Forte, Nicola;Medrihan, Lucian;Cappetti, Beatrice;Baldelli, Pietro;Benfenati, Fabio published 《2-Deoxy-D-glucose enhances tonic inhibition through the neurosteroid-mediated activation of extrasynaptic GABA_A receptors》. 《Epilepsia》published the findings. The article contains the following contents:

Summary : Objective : The inhibition of glycolysis exerts potent antiseizure effects, as demonstrated by the efficacy of ketogenic and low-glucose/nonketogenic diets in the treatment of drug-resistant epilepsy. ATP-sensitive potassium (K_ATP) channels have been initially identified as the main determinant of the reduction of neuronal hyperexcitability. However, a plethora of other mechanisms have been proposed. Herein, we report the ability of 2-deoxy-D-glucose (2-DG), a glucose analog that inhibits glycolytic enzymes, of potentiating γ-aminobutyric acid (GABA)ergic tonic inhibition via neurosteroid-mediated activation of extrasynaptic GABA_A receptors. Methods : Acute effects of 2-DG on the ATP-sensitive potassium currents, GABAergic tonic inhibition, firing activity, and interictal events were assessed in hippocampal slices by whole-cell patch-clamp and local field potential recordings of dentate gyrus granule cells. Results : Acute application of 2-DG activates two distinct outward conductances: a K_ATP channel-mediated current and a bicuculline-sensitive tonic current. The effect of 2-DG on such GABAergic tonic currents was fully prevented by either finasteride or PK11195, which are specific inhibitors of the neurosteroidogenesis pathway acting via different mechanisms. Moreover, the oxidized form of vitamin C, dehydroascorbic acid, known for its ability to induce neurosteroidogenesis, also activated a bicuculline-sensitive tonic current in a manner indistinguishable from that of 2-DG. Finally, we found that the enhancement of K_ATP current by 2-DG primarily regulates intrinsic firing rate of granule cells, whereas the increase of the GABAergic tonic current plays a key role in reducing the frequency of interictal events evoked by treatment of hippocampal slices with the convulsive agent 4-aminopyridine. Significance : We demonstrated, for the first time, that 2-DG potentiates the extrasynaptic tonic GABAergic current through activation of neurosteroidogenesis. Such tonic inhibition represents the main conductance responsible for the antiseizure action of this glycolytic inhibitor.6-Aminonicotinamide (cas: 329-89-5) were involved in the experimental procedure.

6-Aminonicotinamide (cas:329-89-5)Quality Control of 6-Aminonicotinamide is a monocarboxylic acid amide resulting from the formal condensation of the carboxy group of 6-aminonicotinic acid with ammonia. An inhibitor of the NADP(+)-dependent enzyme,6-phosphogluconate dehydrogenase, it interferes with glycolysis.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Li, Zhenbiao;Wei, Yingying;Cao, Zidan;Jiang, Shu;Chen, Yi;Shao, Xingfeng published 《The Jasmonic Acid Signaling Pathway is Associated with Terpinen-4-ol-Induced Disease Resistance against Botrytis cinerea in Strawberry Fruit》 in 2021. The article was appeared in 《Journal of Agricultural and Food Chemistry》. They have made some progress in their research.Recommanded Product: 89-73-6 The article mentions the following:

Terpinen-4-ol, the main component of tea tree oil, markedly increases the disease resistance of postharvest strawberry fruit. To understand the mechanism underlying the enhancement of disease resistance, a high-throughput RNA-seq was used to analyze gene transcription in terpinen-4-ol-treated and untreated fruit. The results show that terpinen-4-ol induces the expression of genes in the jasmonic acid (JA) biosynthesis pathway, secondary metabolic pathways such as phenylpropanoid biosynthesis, and pathways involved in plant-pathogen interactions. Terpinen-4-ol treatment reduced disease incidence and lesion diameter in strawberry fruit inoculated with Botrytis cinerea. Terpinen-4-ol treatment enhanced the expression of genes involved in JA synthesis (FaLOX, FaAOC, and FaOPR3) and signaling (FaCOI1), as well as genes related to disease defense (FaPAL, FaCHI, and FaGLU). In contrast, treatment with the JA biosynthesis inhibitor salicylhydroxamic acid (SHAM) accelerated disease development and inhibited the induction of gene expressions by terpinen-4-ol. We conclude that the JA pathway participates in the induction of disease resistance by terpinen-4-ol in strawberry fruit. More generally, the results illuminate the mechanisms by which disease resistance is enhanced by essential oils. And N,2-Dihydroxybenzamide (cas: 89-73-6) was used in the research process.

N,2-Dihydroxybenzamide(cas: 89-73-6) is a hydroxamic acid that inhibits the activity of p-hydroxybenzoic acid (PHBA) reductase, an enzyme involved in the conversion of PHBA to benzoic acid. Recommanded Product: 89-73-6 The compound has been shown to inhibit mitochondrial membrane potential and mitochondrial functions, leading to cell death.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Candelario, Kate M.;Shuttleworth, C. William;Cunningham, Lee Anna published 《Neural stem/progenitor cells display a low requirement for oxidative metabolism independent of hypoxia inducible factor-1alpha expression》 in 2013. The article was appeared in 《Journal of Neurochemistry》. They have made some progress in their research.Product Details of 329-89-5 The article mentions the following:

Neural stem/progenitor cells (NSPCs) are multipotent cells within the embryonic and adult brain that give rise to both neuronal and glial cell lineages. The maintenance of NSPC multipotency is promoted by low O₂ tension, although the metabolic underpinnings of this trait have not been described. Here, the authors investigated the metabolic state of undifferentiated NSPCs in culture, and tested their relative reliance on oxidative vs. glycolytic metabolism for survival, as well as their dependence on hypoxia inducible factor-1α (HIF-1α) expression for maintenance of metabolic phenotype. Unlike primary neurons, NSPCs from embryonic and adult mice survived prolonged hypoxia in culture. In addition, NSPCs displayed greater susceptibility to glycolytic inhibition compared with primary neurons, even in the presence of alternative mitochondrial TCA substrates. NSPCs were also more resistant than neurons to mitochondrial CN^– toxicity, less capable of utilizing galactose as an alternative substrate to glucose, and more susceptible to pharmacol. inhibition of the pentose phosphate pathway by 6-aminonicotinamide. Inducible deletion of exon 1 of the Hif1a gene improved the ability of NSPCs to utilize pyruvate during glycolytic inhibition, but did not alter other parameters of metabolism, including their ability to withstand prolonged hypoxia. Taken together, these data indicate that NSPCs have a relatively low requirement for oxidative metabolism for their survival and that hypoxic resistance is not dependent upon HIF-1α signaling.6-Aminonicotinamide (cas: 329-89-5) were involved in the experimental procedure.

6-Aminonicotinamide (cas:329-89-5)Product Details of 329-89-5 is an aminopyridine, which is a specific pentose inhibitor and thus inhibits the NADP production.It can be used as a reactant for the synthesis of 6-substituted imidazo[1,2-a]pyridines with potential application as chemotherapeutic drugs.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Zhelev, Zhivko;Ivanova, Donika;Bakalova, Rumiana;Aoki, Ichio;Higashi, Tatsuya published 《Inhibition of the pentose-phosphate pathway selectively sensitizes leukemia lymphocytes to chemotherapeutics by ROS-independent mechanism》. The research results were published in《Anticancer Research》 in 2016.Synthetic Route of C6H7N3O The article conveys some information:

The aim of the present study was to investigate: (i) the possibility of sensitizing leukemia lymphocytes to anticancer drugs by inhibiting pentose-phosphate pathway using 6-aminonicotinamide (6-ANA); (ii) to find combinations with synergistic cytotoxic effect on leukemia lymphocytes and to investigate their cytotoxicity towards normal lymphocytes; (iii) and to clarify the role of reactive oxygen species (ROS) in the induction of apoptosis by those combinations. The study covers 15 anticancer drugs – conventional and new-generation. The experiments were performed on Jurkat leukemia cell line and normal lymphocytes, isolated from clin. healthy blood donors. Four parameters were analyzed simultaneously in both cell suspensions treated by drug or 6-ANA (sep., and in combination): cell viability, induction of apoptosis, level of ROS, and level of protein-carbonyl products. Most combinations of drug plus 6-ANA were characterized by synergistic cytotoxic effects on Jurkat cells. The synergism increased with increasing incubation time. Upon combination of 6-ANA with conventional chemotherapeutic (e.g. doxorubicin), synergistic cytotoxic effects were also detected in normal lymphocytes. In both cell types, the cytotoxicity of the combination of doxorubicin plus 6-ANA was accompanied by increased induction of apoptosis, but by a slight reduction of ROS and protein-carbonyl products compared to cells treated with doxorubicin only. Upon combination of 6-ANA with new-generation anticancer drugs (e.g. everolimus or barasertib), the synergistic cytotoxic effect on leukemia lymphocytes was also accompanied by very strong induction of apoptosis through ROS-independent mechanism(s). Neither of these combinations exhibited any cytotoxicity towards normal lymphocytes. The data suggest that 6-ANA could be used as a supplementary component in anticancer chemotherapy, and would allows therapeutic doses of anticancer drugs to be reduced, thereby minimizing their side-effects. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Synthetic Route of C6H7N3O is an aminopyridine, which is a specific pentose inhibitor and thus inhibits the NADP production.It can be used as a reactant for the synthesis of 6-substituted imidazo[1,2-a]pyridines with potential application as chemotherapeutic drugs.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Gorgun, Murat F.;Zhuo, Ming;Englander, Ella W. published 《Cisplatin Toxicity in Dorsal Root Ganglion Neurons Is Relieved by Meclizine via Diminution of Mitochondrial Compromise and Improved Clearance of DNA Damage》 in 2017. The article was appeared in 《Molecular Neurobiology》. They have made some progress in their research.Application of 329-89-5 The article mentions the following:

Chemotherapy-induced neurotoxicity of peripheral nervous system (PNS) hinders efficacy of cancer treatments. Mechanisms initiating PNS injury by anticancer drugs are incompletely understood delaying development of effective management strategies. To understand events triggered in PNS by cancer drugs, we exposed dorsal root ganglion (DRG) neurons to cisplatin, a drug from platinum-based class of chemotherapeutics frequently implicated in peripheral neuropathies. While cisplatin enters cancer cells and forms cisplatin/DNA crosslinks that block cell proliferation, circulating cisplatin can also reach the PNS and produce crosslinks that impede critical DNA transactions in postmitotic neurons. Cisplatin forms crosslinks with both, nuclear and mitochondrial DNA (mtDNA). Crosslinks are repairable primarily via the nucleotide excision repair (NER) pathway, which is present in nuclei but absent from mitochondrial compartment. Hence, high mitochondrial content and limited shielding by blood nerve barrier make DRG neurons particularly vulnerable to mitochondrial injury by cisplatin. We report that in DRG neurons, cisplatin elevates reactive oxygen species, depletes mtDNA, and impairs mitochondrial respiration, whereas concomitant meclizine supplementation preserves redox balance, attenuates mitochondrial compromise, and augments DNA repair. Meclizine is an antihistamine drug recently implicated in neuroprotection via modulation of energy metabolism Our data demonstrate that in the mitochondria-rich DRG neurons, meclizine mitigates cisplatin-induced mitochondrial compromise via enhancement of pentose phosphate pathway and repletion of NADP (NADPH) and glutathione stores. The findings suggest that meclizine-mediated preservation of redox balance sustains mitochondrial respiration and supports execution of cellular processes, including timely removal of cisplatin crosslinks from nuclear DNA, thereby attenuating cisplatin toxicity in DRG neurons. Collectively, the findings reveal potential for pharmacol. modulation of dorsal root ganglion neurons metabolism for protection against toxicity of chemotherapeutic drugs. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Application of 329-89-5 is an inhibitor of the NADP+-dependent enzyme, PGD (6-phosphogluconate dehydrogenase). Studies have also shown that 6-aminonicotinamide induces apoptosis in tumor cells and causes glial cell degeneration.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Quality Control of 6-Aminonicotinamide《SGK1 signaling promotes glucose metabolism and survival in extracellular matrix detached cells》 was published in 2021. The authors were Mason, Joshua A.;Cockfield, Jordan A.;Pape, Daniel J.;Meissner, Hannah;Sokolowski, Michael T.;White, Taylor C.;Valentin Lopez, Jose C.;Liu, Juan;Liu, Xiaojing;Martinez-Reyes, Inmaculada;Chandel, Navdeep S.;Locasale, Jason W.;Schafer, Zachary T., and the article was included in《Cell Reports》. The author mentioned the following in the article:

Loss of integrin-mediated attachment to extracellular matrix (ECM) proteins can trigger a variety of cellular changes that affect cell viability. Foremost among these is the activation of anoikis, caspase-mediated cell death induced by ECM detachment. In addition, loss of ECM attachment causes profound alterations in cellular metabolism, which can lead to anoikis-independent cell death. Here, we describe a surprising role for serum and glucocorticoid kinase-1 (SGK1) in the promotion of energy production when cells are detached. Our data demonstrate that SGK1 activation is necessary and sufficient for ATP generation during ECM detachment and anchorage-independent growth. More specifically, SGK1 promotes a substantial elevation in glucose uptake because of elevated GLUT1 transcription. In addition, carbon flux into the pentose phosphate pathway (PPP) is necessary to accommodate elevated glucose uptake and PPP-mediated glyceraldehyde-3-phosphate (G3P) is necessary for ATP production Thus, our data show SGK1 as master regulator of glucose metabolism and cell survival during ECM-detached conditions. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Quality Control of 6-Aminonicotinamide is an inhibitor of the NADP+-dependent enzyme, PGD (6-phosphogluconate dehydrogenase). Studies have also shown that 6-aminonicotinamide induces apoptosis in tumor cells and causes glial cell degeneration.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Vimercati, Claudio;Qanud, Khaled;Mitacchione, Gianfranco;Sosnowska, Danuta;Ungvari, Zoltan;Sarnari, Roberto;Mania, Daniella;Patel, Neel;Hintze, Thomas H.;Gupte, Sachin A.;Stanley, William C.;Recchia, Fabio A. published 《Beneficial effects of acute inhibition of the oxidative pentose phosphate pathway in the failing heart》 in 2014. The article was appeared in 《American Journal of Physiology》. They have made some progress in their research.Name: 6-Aminonicotinamide The article mentions the following:

In vitro studies suggested that glucose metabolism through the oxidative pentose phosphate pathway (oxPPP) can paradoxically feed superoxide-generating enzymes in failing hearts. We therefore tested the hypothesis that acute inhibition of the oxPPP reduces oxidative stress and enhances function and metabolism of the failing heart, in vivo. In 10 chronically instrumented dogs, congestive heart failure (HF) was induced by high-frequency cardiac pacing. Myocardial glucose consumption was enhanced by raising arterial glycemia to levels mimicking postprandial peaks, before and after i.v. administration of the oxPPP inhibitor 6-aminonicotinamide (80 mg/kg). Myocardial energy substrate metabolism was measured with radiolabeled glucose and oleic acid, and cardiac 8-isoprostane output was used as an index of oxidative stress. A group of five chronically instrumented, normal dogs served as control. In HF, raising glycemic levels from ∼80 to ∼170 mg/dL increased cardiac isoprostane output by approx. twofold, whereas oxPPP inhibition normalized oxidative stress and enhanced cardiac oxygen consumption, glucose oxidation, and stroke work. In normal hearts glucose infusion did not induce significant changes in cardiac oxidative stress. Myocardial tissue concentration of 6P-gluconate, an intermediate metabolite of the oxPPP, was significantly reduced by ∼50% in treated vs. nontreated failing hearts, supporting the inhibitory effect of 6-aminonicotinamide. Our study indicates an important contribution of the oxPPP activity to cardiac oxidative stress in HF, which is particularly pronounced during common physiol. changes such as postprandial glycemic peaks. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Name: 6-Aminonicotinamide is a well-established inhibitor of the NADP+-dependent enzyme, 6-phosphogluconate dehydrogenase (Ki = 0.46 μM). 6-Aminonicotinamide also reduces cardiovascular oxidative injury following ischemia/reperfusion.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics