Neuroprotective efficacy of poly-arginine R18 and NA-1 (TAT-NR2B9c) peptides following transient middle cerebral artery occlusion in the rat
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We examined the efficacy of R18 in a transient MCAO model and compared its effectiveness to the well-characterized neuroprotective NA-1 peptide. R18 and NA-1 peptides were administered intravenously (30, 100, 300, 1000nmol/kg), 60min after the onset of 90min of MCAO. Infarct volume, cerebral swelling and functional outcomes (neurological score, adhesive tape and rota-rod) were measured 24h after MCAO. R18 reduced total infarct volume by 35.1% (p=0.008), 24.8% (p=0.059), 12.2% and 9.6% for the respective 1000 to 30nmol/kg doses, while the corresponding doses of NA-1 reduced lesion volume by 26.1% (p=0.047), 16.6%, 16.5% and 7%, respectively. R18 also reduced hemisphere swelling by between 46.1% (1000 and 300nmol/kg; p=0.009) and 24.4% (100nmol/kg; p=0.066), while NA-1 reduced swelling by 25.7% (1000nmol/kg; p=0.054). In addition, several R18 and NA-1 treatment groups displayed a significant improvement in at least one parameter of the adhesive tape test. These results confirm the neuroprotective properties of R18, and suggest that the peptide is a more effective neuroprotective agent than NA-1. This provides strong justification for the continuing development of R18 as a neuroprotective treatment for stroke.Keywords:
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Brain and spinal cord (CNS) trauma typically directly kill some neurons leading to permanent neurological deficits. However, they also lead to a number of triggers which in turn frequently kill a vastly larger number of neurons than were killed by the initial insult. The best mechanism for reducing the extent of neurological deficits is to minimize the number of neurons that die immediately due to the trauma, and post-trauma sequelae. Neuroprotection techniques have taken many diverse forms with a breadth too great for a short review. Therefore, this review is focused on the roles of only a small number of neuroprotective agents, with its primary focus being on neuroprotection provided by hypothermia, alone and when combined with the other methods. Included are also recent results involving a novel neuroprotective technique, tested on adult human dorsal root ganglion neurons, comparing the influences of hypothermia and alkalinization singly, providing fourfold and eightfold increases in neuroprotection, respectively, but when combined providing a 26-fold increase in neuroprotection. This combinatorial approach to neuroprotection holds great promise for enhancing the degree of neuroprotection clinically following CNS trauma, leading to the preservation of maximal neurological functions.
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Brain and spinal cord (CNS) trauma typically kill a number of neurons, but even more neurons are killed by secondary causes triggered by the initial trauma. Thus, a minor insult may rapidly cause the death of a vastly larger number of neurons and complete paralysis. The best mechanism for reducing the extent of neurological deficits is to minimize the number of neurons killed by post‐trauma sequelae. Neuroprotection techniques take many diverse forms with a breadth too great for a short review. Therefore, this review focuses on the neuroprotection provided by hypothermia and a number of other neuroprotective techniques, when administered singly or in combination, because it is generally found that combinations of applications lead to significantly better neuroprotection than is achieved by any one alone. The combinatorial approach to neuroprotection holds great promise for enhancing the degree of neuroprotection following trauma, leading to maximum maintenance of neurological function.
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In this paper,by means of confined free swelling test and confined swelling test under loads,redbed mudstone of Shaximiao group in the Middle Jurassic in Chongqing area is present to study its swelling characteristics under confined free and loading conditions,and swelling under different water injections as well.Results reveal that three phases are present in the confined free swelling of mudstone,fast swelling deformation and high swelling increasment in the first phase and increasing swelling velocity in the second phase.95 percent swelling occurs in the former two phases.It is found that vertical loads greatly restrain the confined swelling of mudstone.The confined loading swelling ratios decrease sharply with the increasing vertical loads.Moreover,the amount of water has no obvious effect on swelling characteristic of red bed mudstone within a short time under confined without load,but it plays a controlling role on the stable swelling capacities,swelling processes and characteristics as time lapsing.
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Neuronal cells are extremely vulnerable and have a limited capacity for self-repair in response to injury. For those reasons, there is obvious interest in limiting neuronal damage. Mechanisms and strategies used in order to protect against neuronal injury, apoptosis, dysfunction, and degeneration in the central nervous system are recognized as neuroprotection. Neuroprotection could be achieved through several classes of natural and synthetic neuroprotective agents. However, considering the side effects of synthetic neuroprotective agents, the search for natural neuroprotective agents has received great attention. Recently, an increasing number of studies have identified neuroprotective properties of chitosan and its derivatives; however, there are some significant challenges that must be overcome for the success of this approach. Hence, the objective of this review is to discuss neuroprotective properties of chitosan and its derivatives.
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Herbal bioactive compounds have been investigated to possess neuroprotective properties. They are involved in the modulation of different signaling pathways that may facilitate neuroprotection. In this brief review, some of the promising compounds and their potential neuroprotective effects have been reported. They can be potential sources of therapeutics for neurodegenerative disorders.
KEYWORDS: neuroprotective, herbal, bioactive compounds, neurodegenerative diseases
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Neuroprotective agents are medications that can alter the course of metabolic events and have neuroprotective function. Neuroprotective agents are needed in patients undergoing a surgical procedure and clinical conditions that correspond with the central nervous system (CNS); also, in intensive care, the neuroprotective agents are often used to prevent complications and patient deterioration. Over the years, there is still no clear understanding of the potential for neuroprotection and the interactions between various drugs that serve a crucial role in anesthetic care and critical illness. This literature review will discuss further the mechanism of neuronal damage and various neuroprotective agents.
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