Optimised lyophilisation-based method for different biomolecule single-extractions from the same rat brain sample: Suitability for RNA and protein expression analyses after ischemic stroke

2019 ◽  
Vol 327 ◽  
pp. 108402 ◽  
Author(s):  
Alicia Aliena-Valero ◽  
Sergio Rius-Pérez ◽  
Salvador Pérez ◽  
Germán Torregrosa ◽  
Juan B. Salom
Keyword(s):  
Ischemic Stroke ◽  
Protein Expression ◽  
Rat Brain ◽  
Brain Sample ◽  
Single Extractions

Reduction of ischemic stroke in rat brain by alpha melanocyte stimulating hormone

Neuropeptides ◽  
2008 ◽  
Vol 42 (3) ◽  
pp. 331-338 ◽  
Author(s):  
Gang Chen ◽  
Jørgen Frøkiær ◽  
Michael Pedersen ◽  
Søren Nielsen ◽  
Zhichao Si ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Rat Brain ◽  
Melanocyte Stimulating Hormone ◽  
Stimulating Hormone

scholarly journals Isoflurane/nitrous oxide anesthesia induces increases in NMDA receptor subunit NR2B protein expression in the aged rat brain

2012 ◽  
Vol 1431 ◽  
pp. 23-34 ◽  
Author(s):  
Lana J. Mawhinney ◽  
Juan Pablo de Rivero Vaccari ◽  
Ofelia F. Alonso ◽  
Christopher A. Jimenez ◽  
Concepción Furones ◽  
...  
Keyword(s):  
Nitrous Oxide ◽  
Nmda Receptor ◽  
Protein Expression ◽  
Rat Brain ◽  
Receptor Subunit ◽  
Nmda Receptor Subunit ◽  
Aged Rat ◽  
Oxide Anesthesia

Abstract WP433: Targeting Organic Anion Transporting Polypeptide 1a4 (Oatp1a4) Expression at the Blood-brain Barrier: Implications for Treatment of Ischemic Stroke

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Wazir Abdullahi ◽  
Hrvoje Brzica ◽  
Patrick Ronaldson
Keyword(s):  
Protein Expression ◽  
Western Blot ◽  
Rat Brain ◽  
Blood Brain Barrier ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Organic Anion ◽  
Stroke Treatment ◽  
Brain Microvessels ◽  
Cns Delivery

Introduction: Stroke is a leading cause of mortality and morbidity. Several drugs with neuroprotective properties have been proposed for stroke treatment but many have failed in clinical trials. These failures may be due to limited drug permeability across the blood-brain barrier (BBB). Targeting endogenous BBB uptake transporters (i.e., organic anion transporting polypeptides (Oatps)) is a novel approach that can improve CNS delivery of drugs relevant to stroke therapy (i.e., statins). Optimal CNS drug delivery via Oatp in the setting of stroke requires characterization of regulatory pathways such as transforming growth factor (TGF)-β signaling. The goal of the present study was to investigate, in vivo , involvement of TGF-β signaling via the activin-like kinase (ALK)-1 receptor on Oatp1a4 expression at the BBB. Methods: Female Sprague-Dawley rats (200-250 g) were administered bone morphogenic protein-9 (BMP-9; 0-5 μg/kg, i.p.), an ALK1 agonist, or vehicle (i.e., 0.9% saline). Inhibition experiments were performed using LDN193189 (0-5 mg/kg, i.p.), an ALK1 antagonist. Western blot analysis and fluorescence microscopy of isolated brain microvessels were used to determine protein expression and localization in rat brain microvessels respectively. Results: Fluorescence staining demonstrated localization of Oatp1a4 and ALK1 in rat brain microvessels. Western blot analysis showed a dose dependent increase in Oatp1a4 protein expression in brain microvessels isolated from BMP-9 treated rats as compared to controls. Treatment with 0.5 μg/kg and 5 μg/kg BMP-9 resulted in a 55% and 116% increase in Oatp1a4 protein expression, implying that activation of ALK1 signaling can up-regulate Oatp1a4 at the brain microvasculature. In contrast, 6 h treatment with LDN193189 did not alter Oatp1a4 expression across a dose range of 0-5 mg/kg, suggesting that ALK1 inhibition does not modulate basal Oatp1a4 expression at the BBB. Conclusions: Taken together, our data implies that TGF-β/ALK1 signaling may play a role in altering Oatp1a4 protein expression at the BBB. Studies are currently being undertaken in our laboratory to fully characterize the role of TGF-β/ALK1 signaling in determining CNS delivery of drugs relevant to stroke treatment (i.e., statins).

scholarly journals Cathodal tDCS exerts neuroprotective effect in rat brain after acute ischemic stroke

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Ke-Ying Zhang ◽  
Gang Rui ◽  
Jun-Ping Zhang ◽  
Ling Guo ◽  
Guang-Zhou An ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Rat Brain ◽  
Neuroprotective Effect ◽  
Cathodal Tdcs

scholarly journals Catechol-O-Methyltransferase (COMT) Protein Expression and Activity after Dopaminergic and Noradrenergic Lesions of the Rat Brain

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e61392 ◽  
Author(s):  
Nadia Schendzielorz ◽  
Juha-Pekka Oinas ◽  
Timo T. Myöhänen ◽  
Ilkka Reenilä ◽  
Atso Raasmaja ◽  
...  
Keyword(s):  
Protein Expression ◽  
Rat Brain ◽  
Expression And Activity

scholarly journals Inhibition of the SOCS1-JAK2-STAT3 Signaling Pathway Confers Neuroprotection in Rats with Ischemic Stroke

2017 ◽  
Vol 44 (1) ◽  
pp. 85-98 ◽  
Author(s):  
Xiao-Lei Wang ◽  
Chun-Mei Qiao ◽  
Jiong-Ou Liu ◽  
Chun-Yang Li
Keyword(s):  
Ischemic Stroke ◽  
Protein Expression ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Rat Model ◽  
Caspase 3 ◽  
Neuronal Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Mrna And Protein Expression

Background: The present study aims to investigate the protective effects of the SOCS1-JAK2-STAT3 signaling pathway on neurons in a rat model of ischemic stroke. Methods: Our study was conducted using an ischemic stroke rat model. After the microglia were extracted, 40 neonatal Sprague-Dawley (SD) rats were assigned into the blank, AG490, model and negative control (NC) groups. The neurological function of all the rats was evaluated. Histopathological changes were observed. qRT-PCR and western blotting were applied to measure the expression of genes and proteins in the SOCS1-JAK2-STAT3 signaling pathway and related to apoptosis. The TUNEL assay was conducted to calculate the cellular morphology and apoptosis of neuronal cells. Cell viability was detected using the MTT assay. In addition, immunoassays were used to measure the content of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) as well as the levels of oxidative stress. Results: Compared with the blank group, the model and NC groups showed higher neurological function scores—the cytoplasm of the neurons were cavitated, the organelles were reduced with unclear margins, some of the neurons were necrotic, and apoptosis was increased. In addition, the NC and model groups exhibited decreased cell viability, lower mRNA and protein expression of SOCS1 SOCS3 and bcl-2 and reduced SOD and GSH levels but higher mRNA and protein expression levels of AK2, STAT3,Bax and caspase-3 as well as increased protein expression of P-JAK2, P-STAT3 and activated caspase-3 (c-caspase-3). Moreover, the MDA levels were up-regulated in the NC and model groups. In contrast, opposing trends were found in the AG490 group compared with the NC and model groups. Conclusion: These data demonstrate that inhibiting the SOCS1-JAK2-STAT3 signaling pathway can reduce the loss of nerve function and apoptosis of neuronal cells, which provides a new target for the clinical treatment of ischemic stroke.

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