Alterations in NADPH oxidase expression and blood–brain barrier in bile duct ligation-treated young rats: Effects of melatonin

2012 ◽  
Vol 60 (8) ◽  
pp. 751-758 ◽  
Author(s):  
Yu-Chieh Chen ◽  
Jiunn-Ming Sheen ◽  
You-Lin Tain ◽  
Chih-Cheng Chen ◽  
Miao-Meng Tiao ◽  
...  
Keyword(s):  
Bile Duct ◽  
Nadph Oxidase ◽  
Blood Brain Barrier ◽  
Bile Duct Ligation ◽  
Brain Barrier ◽  
Young Rats ◽  
Blood Brain ◽  
Duct Ligation

scholarly journals Bile acids permeabilize the blood brain barrier after bile duct ligation in rats via Rac1-dependent mechanisms

2014 ◽  
Vol 46 (6) ◽  
pp. 527-534 ◽  
Author(s):  
Matthew Quinn ◽  
Matthew McMillin ◽  
Cheryl Galindo ◽  
Gabriel Frampton ◽  
Hae Yong Pae ◽  
...  
Keyword(s):  
Bile Duct ◽  
Bile Acids ◽  
Blood Brain Barrier ◽  
Bile Duct Ligation ◽  
Brain Barrier ◽  
Blood Brain ◽  
Duct Ligation

scholarly journals Melatonin regulates L-arginine transport and NADPH oxidase in young rats with bile duct ligation: role of protein kinase C

2013 ◽  
Vol 73 (1-4) ◽  
pp. 395-401 ◽  
Author(s):  
You-Lin Tain ◽  
Chih-Cheng Chen ◽  
Chien-Te Lee ◽  
Ying-Hsien Kao ◽  
Jiunn-Ming Sheen ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Bile Duct ◽  
Protein Kinase ◽  
Nadph Oxidase ◽  
Bile Duct Ligation ◽  
Arginine Transport ◽  
Young Rats ◽  
Kinase C ◽  
Duct Ligation

scholarly journals Bile Duct Ligation Upregulates Expression and Function of L-Amino Acid Transporter 1 at Blood–Brain Barrier of Rats via Activation of Aryl Hydrocarbon Receptor by Bilirubin

Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1320
Author(s):  
Xiaoke Zheng ◽  
Hanyu Yang ◽  
Lan Qin ◽  
Siqian Wang ◽  
Lei Xie ◽  
...  
Keyword(s):  
Amino Acid ◽  
Bile Duct ◽  
Liver Failure ◽  
Aryl Hydrocarbon Receptor ◽  
Blood Brain Barrier ◽  
Bile Duct Ligation ◽  
Brain Barrier ◽  
Aryl Hydrocarbon ◽  
Duct Ligation ◽  
And Function

Liver failure is associated with increased levels of brain aromatic amino acids (AAAs), whose transport across the blood–brain barrier (BBB) is mainly mediated by L-amino acid transporter 1 (LAT1). We aimed to investigate whether liver failure induced by bile duct ligation (BDL) increases levels of brain AAAs by affecting the expression and function of LAT1. The LAT1 function was assessed using the brain distribution of gabapentin. It was found that BDL significantly increased levels of gabapentin, phenylalanine, and tryptophan in the cortex, hippocampus, and striatum of rats, and upregulated the expression of total LAT1 protein in hippocampus and striatum as well as cortex membrane LAT1 protein. HCMEC/D3 served as in vitro BBB model, and the data showed that both the serum of BDL rats and bilirubin induced LAT1 expression and function, while bilirubin oxidase almost abolished the upregulation of LAT1 protein by bilirubin and the serum of BDL rats. The enhanced function and expression of LAT1 were also observed in the hippocampus and striatum of hyperbilirubinemia rats. Both aryl hydrocarbon receptor (AhR) antagonist α-naphthoflavone and AhR silencing obviously attenuated the upregulation of LAT1 protein by bilirubin or omeprazole. This study provides the first evidence that BDL upregulates LAT1 at the rat BBB, attributed to the activation of AhR by the increased plasma bilirubin. The results highlight the mechanisms causing BDL-increased levels of brain AAAs and their physiological significance.

Paroxysmal slow cortical activity in Alzheimer’s disease and epilepsy is associated with blood-brain barrier dysfunction

2019 ◽  
Vol 11 (521) ◽  
pp. eaaw8954 ◽  
Author(s):  
Dan Z. Milikovsky ◽  
Jonathan Ofer ◽  
Vladimir V. Senatorov ◽  
Aaron R. Friedman ◽  
Ofer Prager ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Causative Role ◽  
Barrier Dysfunction ◽  
Therapeutic Implications ◽  
Young Rats ◽  
Blood Brain ◽  
Nonconvulsive Seizures

A growing body of evidence shows that epileptic activity is frequent but often undiagnosed in patients with Alzheimer’s disease (AD) and has major therapeutic implications. Here, we analyzed electroencephalogram (EEG) data from patients with AD and found an EEG signature of transient slowing of the cortical network that we termed paroxysmal slow wave events (PSWEs). The occurrence per minute of the PSWEs was correlated with level of cognitive impairment. Interictal (between seizures) PSWEs were also found in patients with epilepsy, localized to cortical regions displaying blood-brain barrier (BBB) dysfunction, and in three rodent models with BBB pathology: aged mice, young 5x familial AD model, and status epilepticus–induced epilepsy in young rats. To investigate the potential causative role of BBB dysfunction in network modifications underlying PSWEs, we infused the serum protein albumin directly into the cerebral ventricles of naïve young rats. Infusion of albumin, but not artificial cerebrospinal fluid control, resulted in high incidence of PSWEs. Our results identify PSWEs as an EEG manifestation of nonconvulsive seizures in patients with AD and suggest BBB pathology as an underlying mechanism and as a promising therapeutic target.

Lack of effects of 1439 MHz electromagnetic near field exposure on the blood-brain barrier in immature and young rats

2005 ◽  
Vol 26 (7) ◽  
pp. 578-588 ◽  
Author(s):  
Masanori Kuribayashi ◽  
Jianqing Wang ◽  
Osamu Fujiwara ◽  
Yuko Doi ◽  
Kyoko Nabae ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Near Field ◽  
Brain Barrier ◽  
Field Exposure ◽  
Young Rats ◽  
Blood Brain
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