Tanshinone IIa Alleviates the Biochemical Changes Associated with Hypoxic Ischemic Brain Damage in a Rat Model

2011 ◽  
Vol 25 (12) ◽  
pp. 1865-1869 ◽  
Author(s):  
Mingyan Hei ◽  
Yali Luo ◽  
Xiaochun Zhang ◽  
Furong Liu
Keyword(s):  
Brain Damage ◽  
Rat Model ◽  
Biochemical Changes ◽  
Tanshinone Iia ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

Significant Role of microRNA-182-5p in Neonatal Hypoxic-Ischemic Injury and Related Mechanism

2020 ◽  
Vol 10 (5) ◽  
pp. 654-661
Author(s):  
Qin Wang ◽  
Ting Wang
Keyword(s):  
Cell Viability ◽  
Brain Tissue ◽  
Brain Damage ◽  
Rat Model ◽  
Target Gene ◽  
Luciferase Reporter ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Qrt Pcr ◽  
The Brain

The purpose of current study was to explore the role and mechanism of microRNA-182-5p (miR182-5p) in neonatal hypoxic ischemic brain damage (HIBD). First, we established a hypoxic-ischemic (HI) rat model and assessed the neurological function of the rats using the Zea Longa score. Then, the level of miR-182-5p in brain tissue of neonatal rats was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Findings revealed that miR-182-5p was significantly down-regulated in the brain tissue of HI rat model. Next, we studied the target gene of miR-182-5p by using TargetScan and dual luciferase reporter assay. Results showed that CASP2 was a direct target gene of miR-182-5p, and the level of CASP2 was significantly up-regulated in the brain tissue of HI rat model. Immediately thereafter, we established an oxygen and glucose deprivation (OGD) cell model of primary cortical neurons, and demonstrated the changes of miR182-5p in cells treated with OGD by qRT-PCR. Finally, to determine the function of miR-182-5p in OGD subjected neuronal cells, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and flow cytometry (FCM) assays were used to study cell viability and apoptosis. The study found that compared with the OGD group, miR-182-5p mimic significantly increased nerve cell viability, reduced cell apoptosis and decreased cleaved-Caspase3/7/8 protein expression, however, all these changes were significantly reversed by overexpression of the CASP2 gene. Taken together, miR-182-5p might protect the nerve cells from ischemia and hypoxia by targeting CASP2, thereby playing a protective role in hypoxic ischemic encephalopathy, which might be a new effective target for neonatal hypoxic ischemic brain damage treatment.

scholarly journals Bilateral Molecular Changes in a Neonatal Rat Model of Unilateral Hypoxic-Ischemic Brain Damage

2006 ◽  
Vol 59 (3) ◽  
pp. 434-439 ◽  
Author(s):  
Evelyn R W van den Tweel ◽  
Annemieke Kavelaars ◽  
Maria Stella Lombardi ◽  
Cora H A Nijboer ◽  
Floris Groenendaal ◽  
...  
Keyword(s):  
Brain Damage ◽  
Rat Model ◽  
Neonatal Rat ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Molecular Changes ◽  
Neonatal Rat Model

A Rat Model for Hypoxic-Ischemic Brain Damage in Very Premature Infants

Neonatology ◽  
1996 ◽  
Vol 69 (5) ◽  
pp. 327-341 ◽  
Author(s):  
Ann Sheldon ◽  
Jing Chuai ◽  
Donna M. Ferriero
Keyword(s):  
Brain Damage ◽  
Premature Infants ◽  
Rat Model ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Very Premature Infants

Combination of deferoxamine and lamotrigine in a rat model of hypoxic-ischemic brain damage

2006 ◽  
Vol 16 ◽  
pp. S6-S7
Author(s):  
G. Papazisis ◽  
D. Kouvelas ◽  
K. Kallaras ◽  
A. Kaiki-Astara ◽  
O. Guiba-Tziampiri
Keyword(s):  
Brain Damage ◽  
Rat Model ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

scholarly journals Interactions between Nitrous Oxide and Tissue Plasminogen Activator in a Rat Model of Thromboembolic Stroke

2011 ◽  
Vol 115 (5) ◽  
pp. 1044-1053 ◽  
Author(s):  
Benoît Haelewyn ◽  
Hélène N. David ◽  
Nathalie Colloc'h ◽  
Denis G. Colomb ◽  
Jean-Jacques Risso ◽  
...  
Keyword(s):  
Nitrous Oxide ◽  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Brain Damage ◽  
Rat Model ◽  
Thromboembolic Stroke ◽  
Subsequent Reduction ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Brain Hemorrhages

Background Preclinical evidence in rodents has suggested that inert gases, such as xenon or nitrous oxide, may be promising neuroprotective agents for treating acute ischemic stroke. This has led to many thinking that clinical trials could be initiated in the near future. However, a recent study has shown that xenon interacts with tissue-type plasminogen activator (tPA), a well-recognized approved therapy of acute ischemic stroke. Although intraischemic xenon inhibits tPA-induced thrombolysis and subsequent reduction of brain damage, postischemic xenon virtually suppresses both ischemic brain damage and tPA-induced brain hemorrhages and disruption of the blood-brain barrier. The authors investigated whether nitrous oxide could also interact with tPA. Methods The authors performed molecular modeling of nitrous oxide binding on tPA, characterized the concentration-dependent effects of nitrous oxide on tPA enzymatic and thrombolytic activity in vitro, and investigated the effects of intraischemic and postischemic nitrous oxide in a rat model of thromboembolic acute ischemic stroke. Results The authors demonstrate nitrous oxide is a tPA inhibitor, intraischemic nitrous oxide dose-dependently inhibits tPA-induced thrombolysis and subsequent reduction of ischemic brain damage, and postischemic nitrous oxide reduces ischemic brain damage, but in contrast with xenon, it increases brain hemorrhages and disruption of the blood-brain barrier. Conclusions In contrast with previous studies using mechanical acute stroke models, these data obtained in a clinically relevant rat model of thromboembolic stroke indicate that nitrous oxide should not be considered a good candidate agent for treating acute ischemic stroke compared with xenon.

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