N 1 ‐(quinolin‐2‐ylmethyl)butane‐1,4‐diamine, a polyamine analogue, attenuated injury in in vitro and in vivo models of cerebral ischemia

2012 ◽  
Vol 30 (7) ◽  
pp. 584-595 ◽  
Author(s):  
Juan Cen ◽  
Lu Liu ◽  
Ling He ◽  
Man Liu ◽  
Chao‐Jie Wang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
In Vivo Models ◽  
Polyamine Analogue

scholarly journals In Vitro and In Vivo Models of Cerebral Ischemia Show Discrepancy in Therapeutic Effects of M2 Macrophages

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e67063 ◽  
Author(s):  
Virginie Desestret ◽  
Adrien Riou ◽  
Fabien Chauveau ◽  
Tae-Hee Cho ◽  
Emilie Devillard ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Therapeutic Effects ◽  
M2 Macrophages ◽  
In Vivo Models

Neuroprotective effects of a new synthetic peptide, CMX-9236, in in vitro and in vivo models of cerebral ischemia

2003 ◽  
Vol 963 (1-2) ◽  
pp. 214-223 ◽  
Author(s):  
Victor E Shashoua ◽  
David S Adams ◽  
Anne Boyer-Boiteau ◽  
Ann Cornell-Bell ◽  
Fuhai Li ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Synthetic Peptide ◽  
Neuroprotective Effects ◽  
In Vivo Models

Opuntia ficus-indica attenuates neuronal injury in in vitro and in vivo models of cerebral ischemia

2006 ◽  
Vol 104 (1-2) ◽  
pp. 257-262 ◽  
Author(s):  
Jung-Hoon Kim ◽  
Shin-Mi Park ◽  
Hyun-Joo Ha ◽  
Chang-Jong Moon ◽  
Tae-Kyun Shin ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Neuronal Injury ◽  
Opuntia Ficus Indica ◽  
In Vivo Models

scholarly journals Cellular Origin and Regulation of D-and L-Serine in in Vitro and in Vivo Models of Cerebral Ischemia

2014 ◽  
Vol 34 (12) ◽  
pp. 1928-1935 ◽  
Author(s):  
Takato Abe ◽  
Masataka Suzuki ◽  
Jumpei Sasabe ◽  
Shinichi Takahashi ◽  
Miyuki Unekawa ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Cultured Cells ◽  
Long Term Potentiation ◽  
Artery Occlusion ◽  
In Vitro Experiments ◽  
In Vivo Models ◽  
Cellular Origin

D-Serine is known to be essential for the activation of the N-methyl-D-aspartate (NMDA) receptor in the excitation of glutamatergic neurons, which have critical roles in long-term potentiation and memory formation. D-Serine is also thought to be involved in NMDA receptor-mediated neurotoxicity. The deletion of serine racemase (SRR), which synthesizes D-Serine from L-Serine, was recently reported to improve ischemic damage in mouse middle cerebral artery occlusion model. However, the cell type in which this phenomenon originates and the regulatory mechanism for D-/L-Serine remain elusive. The D-/L-Serine content in ischemic brain increased until 20 hours after recanalization and then leveled off gradually. The results of in vitro experiments using cultured cells suggested that D-Serine is derived from neurons, while L-Serine seems to be released from astroglia. Immunohistochemistry studies of brain tissue after cerebral ischemia showed that SRR is expressed in neurons, and 3-phosphoglycerate dehydrogenase (3-PGDH), which synthesizes L-Serine from 3-phosphoglycerate, is located in astrocytes, supporting the results of the in vitro experiments. A western blot analysis showed that neither SRR nor 3-PGDH was upregulated after cerebral ischemia. Therefore, the increase in D-/L-Serine was not related to an increase in SRR or 3-PGDH, but to an increase in the substrates of SRR and 3-PGDH.

Protective effects of l-pGlu-(2-propyl)-l-His-l-ProNH2, a newer thyrotropin releasing hormone analog in in vitro and in vivo models of cerebral ischemia

Peptides ◽  
2011 ◽  
Vol 32 (6) ◽  
pp. 1225-1231 ◽  
Author(s):  
Satyendra Kumar Rajput ◽  
Maqsood Ahmad Siddiqui ◽  
Vivek Kumar ◽  
Chhuttan Lal Meena ◽  
Aditya Bhushan Pant ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Thyrotropin Releasing Hormone ◽  
Protective Effects ◽  
In Vivo Models ◽  
Releasing Hormone ◽  
Hormone Analog

scholarly journals Neuroprotective Effects of Insulin-Like Growth Factor-Binding Protein Ligand Inhibitors in Vitro and in Vivo

2003 ◽  
Vol 23 (10) ◽  
pp. 1160-1167 ◽  
Author(s):  
Kenneth B Mackay ◽  
Sarah A Loddick ◽  
Gregory S Naeve ◽  
Alicia M Vana ◽  
Gail M Verge ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Dependent Manner ◽  
Neuroprotective Effects ◽  
In Vivo Models ◽  
Igf I

The role of brain insulin-like growth factors (IGFs) and IGF binding proteins (IGFBPs) in neuroprotection was further investigated using in vitro and in vivo models of cerebral ischemia by assessing the effects of IGF-I, IGF-II, and high affinity IGFBP ligand inhibitors (the peptide [Leu24, 59, 60, Ala31]hIGF-I (IGFBP-LI) and the small molecule NBI-31772 (1-(3,4-dihydroxybenzoyl)-3-hydroxycarbonyl-6, 7-dihydroxyisoquinoline), which pharmacologically displace and elevate endogenous, bioactive IGFs from IGFBPs. Treatment with IGF-I, IGF-II, or IGFBP-LI (2 μg/mL) significantly ( P < 0.05) reduced CA1 damage in organotypic hippocampal cultures resulting from 35 minutes of oxygen and glucose deprivation by 71%, 60%, and 40%, respectively. In the subtemporal middle cerebral artery occlusion (MCAO) model of focal ischemia, intracerebroventricular (icv) administration of IGF-I and IGF-II at the time of artery occlusion reduced ischemic brain damage in a dose-dependent manner, with maximum reductions in total infarct size of 37% ( P < 0.01) and 38% ( P < 0.01), respectively. In this model of MCAO, icv administration of NBI-31772 at the time of ischemia onset also dose-dependently reduced infarct size, and the highest dose (100 μg) significantly reduced both total (by 40%, P < 0.01) and cortical (by 43%, P < 0.05) infarct volume. In the intraluminal suture MCAO model, administration of NBI-31772 (50 μg icv) at the time of artery occlusion reduced both cortical infarct volume (by 40%, P < 0.01) and brain swelling (by 24%, P < 0.05), and it was still effective when treatment was delayed up to 3 hours after the induction of ischemia. These results further define the neuroprotective properties of IGFs and IGFBP ligand inhibitors in experimental models of cerebral ischemia.

Neuroprotective effects of a novel water-soluble poly(ADP-ribose) polymerase-1 inhibitor, MP-124, in in vitro and in vivo models of cerebral ischemia

2011 ◽  
Vol 1389 ◽  
pp. 169-176 ◽  
Author(s):  
Yasuhiro Egi ◽  
Shigeru Matsuura ◽  
Tomoyuki Maruyama ◽  
Masakazu Fujio ◽  
Satoshi Yuki ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Water Soluble ◽  
Neuroprotective Effects ◽  
In Vivo Models ◽  
Soluble Poly

scholarly journals Neuroprotective Effects of Resveratrol in Ischemic Brain Injury

NeuroSci ◽  
2021 ◽  
Vol 2 (3) ◽  
pp. 305-319
Author(s):  
Noelia D. Machado ◽  
Gorka Villena Armas ◽  
Mariana A. Fernández ◽  
Santiago Grijalvo ◽  
David Díaz Díaz
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
De Novo ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
In Vivo Models ◽  
Ischemic Brain ◽  
Number Of Patients

Cerebral ischemia represents the third cause of death and the first cause of disability in adults. This process results from decreasing cerebral blood flow levels as a result of the occlusion of a major cerebral artery. This restriction in blood supply generates low levels of oxygen and glucose, which leads to a decrease in the energy metabolism of the cell, producing inflammation, and finally, neurological deterioration. Currently, blood restoration of flow is the only effective approach as a therapy in terms of ischemic stroke. However, a significant number of patients still have a poor prognosis, probably owing to the increase in the generation of reactive oxygen species (ROS) during the reperfusion of damaged tissue. Oxidative stress and inflammation can be avoided by modulating mitochondrial function and have been identified as potential targets for the treatment of cerebral ischemia. In recent years, the beneficial actions of flavonoids and polyphenols against cerebrovascular diseases have been extensively investigated. The use of resveratrol (RSV) has been shown to markedly decrease brain damage caused by ischemia in numerous studies. According to in vitro and in vivo experiments, there is growing evidence that RSV is involved in several pathways, including cAMP/AMPK/SIRT1 regulation, JAK/ERK/STAT signaling pathway modulation, TLR4 signal transduction regulation, gut/brain axis modulation, GLUT3 up-regulation inhibition, neuronal autophagy activation, and de novo SUR1 expression inhibition. In this review, we summarize the recent outcomes based on the neuroprotective effect of RSV itself and RSV-loaded nanoparticles in vitro and in vivo models focusing on such mechanisms of action as well as describing the potential therapeutic strategies in which RSV plays an active role in cases of ischemic brain injury.

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