benzoic/infarction

Lyen an sove nan clipboard la

Chwazi kalite sòt

Paj 1 soti nan 34 rezilta yo

ARD-353 [4-((2R,5S)-4-(R)-(4-diethylcarbamoylphenyl)(3-hydroxyphenyl)methyl)-2,5-dimethylpiperazin-1-ylmethyl)benzoic acid], a novel nonpeptide delta receptor agonist, reduces myocardial infarct size without central effects.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

A novel delta-receptor selective compound, ARD-353 [4-((2R,5S)-4-(R)-(4-diethylcarbamoylphenyl)(3-hydroxyphenyl)methyl)-2, 5-dimethylpiperazin-1-ylmethyl)benzoic acid], was evaluated for activity on infarct size in a rat model of acute myocardial infarction. ARD-353 was characterized as having delta

Robust neuroprotective effects of 2-((2-oxopropanoyl)oxy)-4-(trifluoromethyl)benzoic acid (OPTBA), a HTB/pyruvate ester, in the postischemic rat brain.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Postischemic brain damage in stroke is proceded with complicated pathological events, and so multimodal drug treatments may offer better therapeutic means for improving clinical outcomes. Here, we report robust neuroprotective effects of a novel compound,

Protective effect of triflusal against acute myocardial infarction in patients with unstable angina: results of a Spanish multicenter trial. Grupo de Estudio del Triflusal en la Angina Inestable.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

A multicenter, double-blind, placebo-controlled study was carried out to evaluate the effect of a new antiplatelet agent, triflusal (2-acetoxy-4-trifluoromethyl benzoic acid), in the prevention of nonfatal myocardial infarction and cardiac or vascular death (principal end-points) in patients with

Inhibition of soluble epoxide hydrolase by trans-4- [4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid is protective against ischemia-reperfusion injury.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Arachidonic acid, a polyunsaturated fatty acid, can be metabolized to cardioprotective epoxyeicosatrienoic acids (EETs) by cytochrome P450 epoxygenases, which are subsequently hydrolyzed to less bioactive dihydroxyeicosatrienoic acids by soluble epoxide hydrolase (sEH). To study the effects of

Inhibition of soluble epoxide hydrolase by cis-4-[4-(3-adamantan-1-ylureido)cyclohexyl-oxy]benzoic acid exhibits antihypertensive and cardioprotective actions in transgenic rats with angiotensin II-dependent hypertension.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

The present study was undertaken to evaluate the effects of chronic treatment with c-AUCB {cis-4-[4-(3-adamantan-1-ylureido)cyclohexyl-oxy]benzoic acid}, a novel inhibitor of sEH (soluble epoxide hydrolase), which is responsible for the conversion of biologically active EETs (epoxyeicosatrienoic

Soluble epoxide hydrolase inhibitor trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid is neuroprotective in rat model of ischemic stroke.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Soluble epoxide hydrolase (sEH) diminishes vasodilatory and neuroprotective effects of epoxyeicosatrienoic acids by hydrolyzing them to inactive dihydroxy metabolites. The primary goals of this study were to investigate the effects of acute sEH inhibition by

Inhibitors of swelling-activated chloride channels increase infarct size and apoptosis in rabbit myocardium.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Apoptosis is a significant contributor to myocardial cell death during ischemia-reperfusion and swelling-activated chloride channels (I(Cl,swell)) contribute to apoptosis. However, the relationship between I(Cl,swell) ischemia-reperfusion and apoptosis remains unknown. To further investigate this,

A Soluble Epoxide Hydrolase Inhibitor Upregulated KCNJ12 and KCNIP2 by Downregulating MicroRNA-29 in a Mouse Model of Myocardial Infarction

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Background: Soluble epoxide hydrolase inhibitors (sEHi) have anti-arrhythmic effects, and we previously found that the novel sEHi t-AUCB (trans-4[-4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid) significantly inhibited

Isoflurane preconditions myocardium against infarction via release of free radicals.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND Isoflurane exerts cardioprotective effects that mimic the ischemic preconditioning phenomenon. Generation of free radicals is implicated in ischemic preconditioning. The authors investigated whether isoflurane-induced preconditioning may involve release of free radicals. METHODS Sixty-one

Circulating microparticles from patients with myocardial infarction cause endothelial dysfunction.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND Shed membrane microparticles circulate in the peripheral blood of nonischemic (NI) patients and patients with myocardial infarction (MI). We investigated whether or not these microparticles would affect endothelium-dependent responses. RESULTS Rat aortic rings with endothelium were

Soluble epoxide hydrolase inhibitors, t-AUCB, downregulated miR-133 in a mouse model of myocardial infarction.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND It has been demonstrated that soluble epoxide hydrolase inhibitors (sEHIs) are protective against ischemia-induced lethal arrhythmias, but the mechanisms involved are unknown. Previously, we showed that sEHIs might reduce the incidence of ischemic arrhythmias by suppressing microRNA-1

Beneficial effects of cardiac chymase inhibition during the acute phase of myocardial infarction.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Recently, the presence of the chymase-dependent angiotensin (Ang) II-generating system in hamsters, dogs, monkeys, as well as human cardiovascular tissues has been identified. We have reported that the activation of cardiac chymase was more prominent than that of angiotensin converting enzyme (ACE)

Rescue of neurons from ischemic injury by peroxisome proliferator-activated receptor-gamma requires a novel essential cofactor LMO4.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Activation of peroxisome proliferator-activated receptor-gamma (PPARgamma) signaling after stroke may reduce brain injury, but this effect will depend on the levels of receptor and cofactors. Here, we showed that the direct effect of PPARgamma signaling to protect neurons from ischemic injury

Peroxynitrite induces HMGB1 release by cardiac cells in vitro and HMGB1 upregulation in the infarcted myocardium in vivo.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE High-mobility group box 1 (HMGB1) is a nuclear protein actively secreted by immune cells and passively released by necrotic cells that initiates pro-inflammatory signalling through binding to the receptor for advance glycation end-products. HMGB1 has been established as a key inflammatory

Chloride channel inhibition blocks the protection of ischemic preconditioning and hypo-osmotic stress in rabbit ventricular myocardium.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

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

Antre nan paj
facebook nou an

Herbal & Natural Medicine

Baz done ki pi konplè remèd fèy medsin te apiye nan syans

Travay nan 55 lang
Geri èrbal te apiye nan syans
Remèd fèy rekonesans pa imaj
Kat entèaktif GPS - tag zèb sou kote (vini byento)
Li piblikasyon syantifik ki gen rapò ak rechèch ou an
Search remèd fèy medsin pa efè yo
Izeganize enterè ou yo ak rete kanpe fè dat ak rechèch la nouvèl, esè klinik ak rive

Tape yon sentòm oswa yon maladi epi li sou remèd fèy ki ta ka ede, tape yon zèb ak wè maladi ak sentòm li itilize kont.
* Tout enfòmasyon baze sou rechèch syantifik pibliye