scholarly journals Effect of curcumin in the acute phase of ischemia in chronic cerebral hypoperfusion in rats

2018 ◽  
Vol 17 (1) ◽  
pp. 69-73
Author(s):  
N. S. Shcherbak ◽  
M. A. Popovetskiy ◽  
G. Yu. Yukina ◽  
M. M. Galagudza
Keyword(s):  
Brain Injury ◽  
Acute Phase ◽  
Wistar Rats ◽  
Neuroprotective Effect ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Ischemic Brain Injury ◽  
Protective Effects ◽  
Single Application ◽  
Ischemic Brain

Curcumin presents antioxidant and anti-inflammatory properties and can be considered as a neuroprotector. Data on doses and duration of application of curcumin to achieve protective effects in various types of ischemic brain injury is controversial. The purpose was to study the neuroprotective properties of curcumin in the acute phase of ischemia in chronic cerebral hypoperfusion in rats. It is shown that a single application of curcumin (300 mg/kg, i.p.) is not has neuroprotective effect in the acute phase of ischemia in chronic hypoperfusion in Wistar rats. The results allow to conclude that the neuroprotective effect of a single application of curcumin.

Protective effects of melatonin in ischemic brain injury

2000 ◽  
Vol 29 (4) ◽  
pp. 217-227 ◽  
Author(s):  
Salvatore Cuzzocrea ◽  
Giuseppina Costantino ◽  
Eloisa Gitto ◽  
Emanuela Mazzon ◽  
Francesco Fulia ◽  
...  
Keyword(s):  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Protective Effects ◽  
Ischemic Brain

Protective effects of FGF10 on neurovascular unit in a rat model of neonatal hypoxic-ischemic brain injury

2020 ◽  
Vol 332 ◽  
pp. 113393
Author(s):  
Mingchu Fang ◽  
Shishuang Jiang ◽  
Jianghu Zhu ◽  
Xiaoqin Fu ◽  
Yingying Hu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Rat Model ◽  
Neurovascular Unit ◽  
Ischemic Brain Injury ◽  
Protective Effects ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

scholarly journals Hydrogen Gas Attenuates Hypoxic-Ischemic Brain Injury via Regulation of the MAPK/HO-1/PGC-1a Pathway in Neonatal Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-16 ◽  
Author(s):  
Peipei Wang ◽  
Mingyi Zhao ◽  
Zhiheng Chen ◽  
Guojiao Wu ◽  
Masayuki Fujino ◽  
...  
Keyword(s):  
Brain Injury ◽  
Protein Kinase ◽  
Pc12 Cells ◽  
Heme Oxygenase 1 ◽  
Ischemic Brain Injury ◽  
Protective Effects ◽  
Neonatal Rats ◽  
Ischemic Brain ◽  
Differentiated Pc12 Cells ◽  
Hypoxic Ischemic Brain Injury

Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of death in neonates with no effective treatments. Recent advancements in hydrogen (H2) gas offer a promising therapeutic approach for ischemia reperfusion injury; however, the impact of this approach for HIE remains a subject of debate. We assessed the therapeutic effects of H2 gas on HIE and the underlying molecular mechanisms in a rat model of neonatal hypoxic-ischemic brain injury (HIBI). H2 inhalation significantly attenuated neuronal injury and effectively improved early neurological outcomes in neonatal HIBI rats as well as learning and memory in adults. This protective effect was associated with initiation time and duration of sustained H2 inhalation. Furthermore, H2 inhalation reduced the expression of Bcl-2-associated X protein (BAX) and caspase-3 while promoting the expression of Bcl-2, nuclear factor erythroid-2-related factor 2, and heme oxygenase-1 (HO-1). H2 activated extracellular signal-regulated kinase and c-Jun N-terminal protein kinase and dephosphorylated p38 mitogen-activated protein kinase (MAPK) in oxygen-glucose deprivation/reperfusion (OGD/R) nerve growth factor-differentiated PC12 cells. Inhibitors of MAPKs blocked H2-induced HO-1 expression. HO-1 small interfering RNA decreased the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and sirtuin 1 (SIRT1) and reversed the protectivity of H2 against OGD/R-induced cell death. These findings suggest that H2 augments cellular antioxidant defense capacity through activation of MAPK signaling pathways, leading to HO-1 expression and subsequent upregulation of PGC-1α and SIRT-1 expression. Thus, upregulation protects NGF-differentiated PC12 cells from OGD/R-induced oxidative cytotoxicity. In conclusion, H2 inhalation exerted protective effects on neonatal rats with HIBI. Early initiation and prolonged H2 inhalation had better protective effects on HIBI. These effects of H2 may be related to antioxidant, antiapoptotic, and anti-inflammatory responses. HO-1 plays an important role in H2-mediated protection through the MAPK/HO-1/PGC-1α pathway. Our results support further assessment of H2 as a potential therapeutic for neurological conditions in which oxidative stress and apoptosis are implicated.

scholarly journals CYP3A Excipient-Based Microemulsion Prolongs the Effect of Magnolol on Ischemia Stroke Rats

Pharmaceutics ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 737 ◽  
Author(s):  
Jiun-Wen Guo ◽  
Chih-Cheng Chien ◽  
Jiann-Hwa Chen
Keyword(s):  
Brain Injury ◽  
Water Solubility ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
Microemulsion Formulation ◽  
Brain Infarct ◽  
Time Curve ◽  
Release Formulation ◽  
Ischemic Brain ◽  
Effective Delivery

Magnolol, which is a CYP3A substrate, is a well-known agent that can facilitate neuroprotection and reduce ischemic brain damage. However, a well-controlled release formulation is needed for the effective delivery of magnolol due to its poor water solubility. In this study, we have developed a formulation for a CYP3A-excipient microemulsion, which can be administrated intraperitoneally to increase the solubility and bioavailability of magnolol and increase its neuroprotective effect against ischemic brain injury. The results showed a significant improvement in the area under the plotted curve of drug concentration versus time curve (AUC0–t) and mean residence time (MRT) of magnolol in microemulsion compared to when it was dissolved in dimethyl sulfoxide (DMSO). Both magnolol in DMSO and microemulsion, administrated after the onset of ischemia, showed a reduced visual brain infarct size. As such, this demonstrates a therapeutic effect on ischemic brain injury caused by occlusion, however it is important to note that a pharmacological effect cannot be concluded by this study. Ultimately, our study suggests that the excipient inhibitor-based microemulsion formulation could be a promising concept for the substrate drugs of CYP3A.

Multiple actions of the coumarine derivative cloricromene and its protective effects on ischemic brain injury

1995 ◽  
Vol 351 (2) ◽  
Author(s):  
Gioacchino Calapai ◽  
Francesco Squadrito ◽  
Antonio Rizzo ◽  
MariaC. Marciano ◽  
GiuseppeM. Campo ◽  
...  
Keyword(s):  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Protective Effects ◽  
Ischemic Brain

Ischemic brain injury in vitro: protective effects of NMDA receptor antagonists and calmidazolium

1990 ◽  
Vol 528 (1) ◽  
pp. 133-137 ◽  
Author(s):  
Roman Pohorecki ◽  
Gerald L. Becker ◽  
Pamela J. Reilly ◽  
Dennis F. Landers
Keyword(s):  
Brain Injury ◽  
Nmda Receptor ◽  
Ischemic Brain Injury ◽  
Nmda Receptor Antagonists ◽  
Protective Effects ◽  
Receptor Antagonists ◽  
Ischemic Brain

Neuroprotective effect of human placental extract on hypoxic–ischemic brain injury in neonatal rats

2013 ◽  
Vol 35 (1) ◽  
pp. 68-74 ◽  
Author(s):  
Jee Yoon Park ◽  
Jung Hye Byeon ◽  
Sung-Won Park ◽  
So-Hee Eun ◽  
Kyu Young Chae ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
Neonatal Rats ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
Placental Extract

scholarly journals The Acute-Phase Protein PTX3 is an Essential Mediator of Glial Scar Formation and Resolution of Brain Edema after Ischemic Injury

2013 ◽  
Vol 34 (3) ◽  
pp. 480-488 ◽  
Author(s):  
Beatriz Rodriguez-Grande ◽  
Matimba Swana ◽  
Loan Nguyen ◽  
Pavlos Englezou ◽  
Samaneh Maysami ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Edema ◽  
Acute Phase ◽  
Acute Phase Protein ◽  
Ischemic Injury ◽  
Glial Scar ◽  
Scar Formation ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Phase Protein

Acute-phase proteins (APPs) are key effectors of the immune response and are routinely used as biomarkers in cerebrovascular diseases, but their role during brain inflammation remains largely unknown. Elevated circulating levels of the acute-phase protein pentraxin-3 (PTX3) are associated with worse outcome in stroke patients. Here we show that PTX3 is expressed in neurons and glia in response to cerebral ischemia, and that the proinflammatory cytokine interleukin-1 (IL-1) is a key driver of PTX3 expression in the brain after experimental stroke. Gene deletion of PTX3 had no significant effects on acute ischemic brain injury. In contrast, the absence of PTX3 strongly compromised blood–brain barrier integrity and resolution of brain edema during recovery after ischemic injury. Compromised resolution of brain edema in PTX3-deficient mice was associated with impaired glial scar formation and alterations in scar-associated extracellular matrix production. Our results suggest that PTX3 expression induced by proinflammatory signals after ischemic brain injury is a critical effector of edema resolution and glial scar formation. This highlights the potential role for inflammatory molecules in brain recovery after injury and identifies APPs, in particular PTX3, as important targets in ischemic stroke and possibly other brain inflammatory disorders.

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