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Leht 1 alates 80 tulemused
Combination treatment with N-acetyl-seryl-aspartyl-lysyl-proline and tissue plasminogen activator provides potent neuroprotection in rats after stroke.
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OBJECTIVE
N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), an endogenously produced circulating peptide in humans and rodents, exerts anti-inflammatory and cardioprotective activities in various cardiovascular diseases.
METHODS
The present study evaluated the neuroprotective effect of AcSDKP alone
'Five at one stroke': proline and small peptides in the stereoselective de novo synthesis and enantiotopic functionalization of carbohydrates.
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Asymmetric catalysis with the simple amino acid proline (so called 'enamine catalysis') arrested big attention in the last few years since the re-discovery of the Hajos-Parrish-Eder-Sauer-Wiechert reaction. After basic mechanistic studies, probing scope and limitations of the catalyst and the
Matrix-derived inflammatory mediator N-acetyl proline-glycine-proline is neurotoxic and upregulated in brain after ischemic stroke.
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BACKGROUND
N-acetyl proline-glycine-proline (ac-PGP) is a matrix-derived chemokine produced through the proteolytic destruction of collagen by matrix metalloproteinases (MMPs). While upregulation and activation of MMPs and concomitant degradation of the extracellular matrix are known to be
N-Acetyl-Seryl-Aspartyl-Lysyl-Proline Augments Thrombolysis of tPA (Tissue-Type Plasminogen Activator) in Aged Rats After Stroke.
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Background and Purpose- Stroke is a leading cause of disability worldwide, mainly affecting the elderly. However, preclinical studies in aged ischemic animals are limited. N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is a naturally occurring tetrapeptide with vascular-protective properties. The
Plasma cyclic glycine proline/IGF-1 ratio predicts clinical outcome and recovery in stroke patients.
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Neuroprotective role of a proline-rich Akt substrate in apoptotic neuronal cell death after stroke: relationships with nerve growth factor.
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The Akt signaling pathway contributes to regulation of apoptosis after a variety of cell death stimuli. A novel proline-rich Akt substrate (PRAS) was recently detected and found to be involved in apoptosis. In our study, Akt activation was modulated by growth factors, and treatment with nerve growth
Memory restoring and neuroprotective effects of the proline-containing dipeptide, GVS-111, in a photochemical stroke model.
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Local thrombosis of the frontal cortex (Fr1 and Fr3 fields), caused by combination of the intravenous photosensitive dye Rose Bengal administration with focused high-intensity illumination of the frontal bone, was shown to provoke a pronounced deficit in step-through passive avoidance performance in
Acute vasodepressor effect of D-3-mercapto-2-methylpropanoyl-L-proline (SQ 14,225) in the stroke-prone substrain of spontaneously hypertensive rats (SHRSP).
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Chronic treatment with captopril, SQ29,852, hydralazine and a 33% fish meal diet in malignant stroke-prone spontaneously hypertensive rats.
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Malignant stroke-prone spontaneously hypertensive rats (M-SHRSP) are a useful animal model for studying juvenile malignant hypertension. Using M-SHRSP males, the effects of SQ 29,852 [(S)-1-[6-amino-2-[[hydroxy (4-phenylbutyl) phosphinyl]oxy]-1-oxohexyl]-L-proline; 30-40 mg/kg per day], captopril
Proline-containing peptides-New insight and implications: A Review.
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The family of regulatory proline-containing peptides (PCPs), also known as glyprolines, exhibit significant biological activity. The group of glyprolines includes Gly-Pro (GP), Pro-Gly-Pro (PGP), cyclic Gly-Pro (cGP), as well as PGP derivatives, for example, N-acetylated PGP (N-a-PGP) and
MRI evaluation of BBB disruption after adjuvant AcSDKP treatment of stroke with tPA in rat.
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The primary limitation of thrombolytic treatment of ischemic stroke with tissue plasminogen activator (tPA) is the hemorrhagic risk. We tested AcSDKP (N-acetyl-seryl-aspartyl-lysyl-proline), as an auxiliary therapeutic agent, to reduce blood-brain barrier (BBB) disruption in a combination tPA
NNZ-2566: a Gly-Pro-Glu analogue with neuroprotective efficacy in a rat model of acute focal stroke.
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The N-terminal cleavage product of human insulin-like growth factor-1 (IGF-1) in the brain is the tripeptide molecule Glypromate (Gly-Pro-Glu). Glypromate has demonstrated neuroprotective effects in numerous in vitro and in vivo models of brain injury and is in clinical trials for the prevention of
Normal cardiac contraction in mice lacking the proline-alanine rich region and C1 domain of cardiac myosin binding protein C.
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Cardiac myosin binding protein C (cMyBP-C) is an essential regulator of cross bridge cycling. Through mechanisms that are incompletely understood the N-terminal domains (NTDs) of cMyBP-C can activate contraction even in the absence of calcium and can also inhibit cross bridge kinetics in the
Voltage sensitivity and conformational change of isolated S4L45 fragments from sodium channels are tuned to proline.
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Peptide fragments reproducing the sequences of S4 segments extended with L45 linkers from the four homologous domains of the electric eel sodium channel were chemically synthesized and purified to allow circular dichroism studies in various solvents and conductance assays in planar lipid bilayers.
Molecular basis for proline- and arginine-rich peptide inhibition of proteasome.
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PR39, a naturally occurring and cell-permeable proline- and arginine-rich peptide, blocks the degradation of inhibitor of nuclear factor kappaB (IkappaBalpha), thereby attenuating inflammation. It is a noncompetitive and reversible inhibitor of 20S proteasome. To identify its basis of action, we
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