Taurine attenuates inflammatory response following cerebral ischemia and reperfusion

2015 ◽  
Vol 411 (422) ◽  
pp. 411-422
Author(s):  
Katarina Matthes ◽  
Felix Niggli ◽  
Toshihiko Wakabayashi
Keyword(s):  
Cerebral Ischemia ◽  
Inflammatory Cytokines ◽  
Infarct Volume ◽  
Transient Cerebral Ischemia ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Cerebral Ischemia And Reperfusion ◽  
The Central Nervous System ◽  
Pro Inflammatory Cytokines

Taurine is a kind of endogenous free amino acid in tissue and a potent antioxidant agent its function may in part be to adjust calcium homeostasis in cells, anti-oxidative stress, anti-inflammatory and cell protector but little is known about the expression or the role of Taurine in the central nervous system. Stroke is the major cause of death and disability worldwide. Here, we investigated the role of Taurine in ischemic stroke as a potential neuroprotective using rat model of transient cerebral ischemia. Transient cerebral ischemia was induced by MCAO were performed on male Sprague-Dawley rats. TTC staining used to measurement of infarct volume in the brain and ELISA kits to assay cytokines. Our data suggested that Taurine reduced cerebral infarct size, decreased pro-inflammatory cytokines expression and produced lower level of ICAM-1. These results suggest that Taurine can be exerting significantly protective effect against brain ischemic injury through inhibiting pro-inflammatory cytokines and ICAM-1.

scholarly journals Effects of Gentianine on the Production of Pro-inflammatory Cytokines in Male Sprague-Dawley Rats Treated with Lipopolysaccharide (LPS)

2005 ◽  
Vol 28 (4) ◽  
pp. 750-753 ◽  
Author(s):  
Wie-Jong Kwak ◽  
Joo-Hyon Kim ◽  
Keun-Ho Ryu ◽  
Yong-Baik Cho ◽  
Sun-Duck Jeon ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Pro Inflammatory Cytokines

Retinal A2A and A3 adenosine receptors modulate the components of the rat electroretinogram

2017 ◽  
Vol 34 ◽  
Author(s):  
GUDMUNDUR JONSSON ◽  
THOR EYSTEINSSON
Keyword(s):  
Adenosine Receptors ◽  
Mean Amplitude ◽  
Oscillatory Potentials ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Single Flash ◽  
The Central Nervous System ◽  
Photopic Erg ◽  
The Mean

AbstractAdenosine is a neuromodulator present in various areas of the central nervous system, including the retina. Adenosine may serve a neuroprotective role in the retina, based on electroretinogram (ERG) recordings from the rat retina. Our purpose was to assess the role of A2A and A3 adenosine receptors in the generation and modulation of the rat ERG. The flash ERG was recorded with corneal electrodes from Sprague Dawley rats. Agonists and antagonists for A2A and A3 receptors, and adenosine were injected (5 µl) into the vitreous. The effects on the components of the single flash scotopic and photopic ERGs were examined, and ERG flicker. Adenosine (0.5 mM) increased the mean amplitudes of the scotopic ERG a-waves (68 ± 8 to 97 ± 14 µV, P = 0.042), and b-waves (236 ± 38 µV to 305 ± 42 µV). A2A agonist CGS21680 (2 mM) reduced the mean amplitude of the ERG b-wave, from 298 ± 21 µV in response to the brightest stimulus to 212 ± 19 µV (P = 0.005), and mean scotopic oscillatory potentials (OPs) from 100 ± 9 µV to 47 ± 11 µV (P = 0.023). ZM241385 [4 mM], an A2A antagonist, decreased the scotopic b-wave of the ERG. A3 agonist 2-CI-IB-MECA (0.5 mM) increased the a-wave, while decreasing the scotopic and photopic ERG b-waves, and the scotopic OPs. A3 antagonist VUF5574 (1 mM) increased the mean amplitude of the scotopic a-wave (66 ± 8 to 140 ± 29 µV, P = 0.046) and b-wave (224 ± 20 to 312 ± 39 µV, P = 0.0037). No significant effects on ERG flicker were found. We conclude that retinal neurons containing A2A and/or A3 adenosine receptors contribute to the generation of the ERG a- and b-waves and OPs.

Role of the immune response in the pathogenesis of Alzheimer’s disease and possibilities of anti-inflammatory therapy

2021 ◽  
Vol LII (3) ◽  
pp. 55-62
Author(s):  
Sergey V. Vorobev ◽  
Andrey Yu. Emelin ◽  
Raisa N. Kuznetsova ◽  
Igor V. Kudryavtsev
Keyword(s):  
Inflammatory Cytokines ◽  
Therapeutic Potential ◽  
Main Role ◽  
Markers Of Inflammation ◽  
Alternative Hypotheses ◽  
The Central Nervous System ◽  
Anti Inflammatory ◽  
T Helpers ◽  
Pro Inflammatory Cytokines

In modern scientific society several alternative hypotheses for the formation of Alzheimers disease are considered, proposed on the basis of data obtained as a result of research. In almost any of them, the development of an immuno-inflammatory response is discussed as one of the main pathogenic mechanisms of the disease. It was found that the development of neurodegeneration is accompanied by the accumulation of pro-inflammatory cytokines and other markers of inflammation in the peripheral blood and brain tissues. At the same time, the obtained results suggest that the main role in pathogenesis may be played by T-helpers of the Th17 population that can penetrate the blood-brain barrier. In addition, microglia, which is the main immune-presenting component of the central nervous system, and astrocytes, which are capable of excessive production of pro- inflammatory cytokines and regulation of -amyloid clearance, are considered as key components in these reactions. Based on these data, attempts are being made to develop drugs that have an anti-inflammatory effect and can positively influence the dynamics of the disease. The initial results obtained in some cases demonstrate a certain positive effect, which suggests that there is a therapeutic potential for this type of therapy.

scholarly journals A20-Binding Inhibitor of NF-κB 1 Ameliorates Neuroinflammation and Mediates Antineuroinflammatory Effect of Electroacupuncture in Cerebral Ischemia/Reperfusion Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Xueling Zhou ◽  
Wenhao Lu ◽  
You Wang ◽  
Jiani Li ◽  
Yong Luo
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Neurological Deficits ◽  
Sprague Dawley ◽  
Cerebral Ischemia Reperfusion ◽  
Neuroprotective Strategy

A20-binding inhibitor of NF-κB 1 (ABIN1) is an inhibitor of NF-κB and exerts anti-inflammatory effect. Electroacupuncture (EA) is considered as a neuroprotective strategy by inhibiting neuroinflammatory damage after cerebral ischemia. This study was performed to explore the role of ABIN1 and investigate whether the ABIN1 is involved in the mechanism of EA in cerebral ischemia/reperfusion (I/R) rats. Male Sprague-Dawley (SD) rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) and received EA after reperfusion once a day. Lentivirus-mediated ABIN1 gene knockdown was used to detect the role of ABIN1 in neuroinflammation after I/R. ABIN1 expression, proinflammatory cytokine levels, microglial activation, neurological function, infarct volumes, and NF-κB activation were assessed. ABIN1 expression was elevated in the peri-infarct cortex and was further upregulated by EA. ABIN1 knockdown increased the levels of proinflammatory cytokines and activation of microglia, worsened neurological deficits, and enlarged the infarct volume. Moreover, ABIN1 was blocked to partially reverse the neuroprotective effect of EA, and this treatment weakened the ability of EA to suppress NF-κB activity. Based on these findings, ABIN1 is a potential suppressor of neuroinflammation and ABIN1 mediates the antineuroinflammatory effect of EA in cerebral I/R rats.

Abstract MP05: Pvn-specific Microgliosis And Inflammation Precedes Sympathoexcitation In gαI 2 Protein-dependent, Salt-sensitive Hypertension

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Jesse D Moreira ◽  
Parul Chaudhary ◽  
Kayla M Nist ◽  
Richard D Wainford
Keyword(s):  
Inflammatory Cytokines ◽  
Paraventricular Nucleus ◽  
Whole Blood ◽  
Microglial Activation ◽  
Sprague Dawley ◽  
Cardiac Perfusion ◽  
Osmotic Minipumps ◽  
Sprague Dawley Rats ◽  
Salt Sensitive Hypertension ◽  
Pro Inflammatory Cytokines

Aim: Hypothalamic paraventricular nucleus (PVN) Gαi 2 proteins mediate sympathoinhibitory responses to a high salt (HS; 4% NaCl) diet. Failure to upregulate Gαi 2 proteins in response to a HS diet results in PVN inflammation and salt sensitive hypertension (SSHTN). We hypothesize that microglial-mediated PVN inflammation precedes sympathoexcitation in Gαi 2 protein-dependent SSHTN. Methods: Three-month-old male Sprague Dawley rats implanted with ICV cannulas fitted to osmotic minipumps to centrally infuse either a control scrambled (SCR) oligodeoxynucleotide (ODN) or a Gαi 2 targeted ODN, which downregulates CNS Gαi 2 proteins by ~85%, (25μg/5μl/day/ODN) were placed on a 1-7-day normal salt (NS; 0.6% NaCl) or HS diet (n=5/group) and underwent cardiac perfusion. Brain immunohistochemistry was used to assess PVN and subfornical organ microgliosis and qualitatively assess levels of PVN pro-inflammatory cytokines (PIC) IL-1β, IL-6, and TNFα. In additional groups, MAP was assessed via radiotelemetry, and whole blood and kidneys were obtained for ELISA measurement of plasma and renal norepinephrine (NE) as estimates of sympathetic tone. Results: By 24h in control SCR ODN infused rats a HS diet, which did not alter MAP or microglial activation, evoked sympathoinhibition. In contrast, in Gαi 2 ODN infused rats a HS diet did not result in sympathoinhibition and evoked significant increases in MAP, PVN microgliosis and PVN PIC expression within 24h, and elevated renal NE content by Day 3. Conclusions: Our data suggest that in the male Sprague-Dawley model of PVN Gαi 2 protein-dependent SSHTN PVN inflammation (microgliosis and PIC production) precedes sympathoexcitation.

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