scholarly journals Oxytocin Mediates Social Neuroprotection After Cerebral Ischemia

Stroke ◽  
2011 ◽  
Vol 42 (12) ◽  
pp. 3606-3611 ◽  
Author(s):  
Kate Karelina ◽  
Kathleen A. Stuller ◽  
Brant Jarrett ◽  
Ning Zhang ◽  
Jackie Wells ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Receptor Antagonist ◽  
Social Housing ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
Experimental Stroke ◽  
Stroke Outcome ◽  
Socially Isolated ◽  
Cerebral Artery Occlusion ◽  
And Oxidative Stress

Background and Purpose— The reduced incidence, morbidity, and mortality of stroke among humans with strong social support have been well-documented; however, the mechanisms underlying these socially mediated phenomena remain unknown, but may involve oxytocin (OT), a hormone that modulates some aspects of social behavior in humans and other animals. Methods— In the present study, adult male mice were socially isolated (housed individually) or socially paired (housed with an ovariectomized female); social pairing increased hypothalamic OT gene expression. To determine whether a causal relationship exists between increased OT and improved stroke outcome, mice were treated with exogenous OT or OT receptor antagonist beginning 1 week before induction of experimental stroke via middle cerebral artery occlusion. Results— Relative to social isolation, social housing attenuated infarct size, neuroinflammation, and oxidative stress following experimental stroke; the neuroprotective effect of social housing was eliminated by receptor antagonist treatment. In contrast, administration of OT to socially isolated mice reproduced the neuroprotection conferred by social housing. We further report evidence for a direct suppressive action of OT on cultured microglia, which is a key instigator in the development of neuroinflammation after cerebral ischemia. Conclusions— These findings support the hypothesis that OT mediates the neuroprotective effect of social interaction on stroke outcome.

scholarly journals Adenosine A1 Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

2004 ◽  
Vol 24 (7) ◽  
pp. 771-779 ◽  
Author(s):  
Mitsuyoshi Yoshida ◽  
Kazuhiko Nakakimura ◽  
Ying Jun Cui ◽  
Mishiya Matsumoto ◽  
Takefumi Sakabe
Keyword(s):  
Cerebral Ischemia ◽  
Receptor Antagonist ◽  
Channel Blocker ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
A1 Receptor ◽  
Cerebral Artery Occlusion ◽  
Development Of Tolerance

Involvement of adenosine and adenosine triphosphate-sensitive potassium (KATP) channels in the development of ischemic tolerance has been suggested in global ischemia, but has not been studied extensively in focal cerebral ischemia. This study evaluated modulating effects of adenosine A1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) and mitochondrial KATP channel blocker 5HD (5-hydroxydecanoate) on the development of tolerance to focal cerebral ischemia in rats. Preconditioning with 30-minute middle cerebral artery occlusion (MCAO) reduced cortical and subcortical infarct volume following 120-minute MCAO (test ischemia) given 72 hours later. The neuroprotective effect of preconditioning was attenuated by 0.1 mg/kg DPCPX given before conditioning ischemia (30-minute MCAO), but no influence was provoked when it was administered before test ischemia. DPCPX had no effect on infarct volume after conditioning or test ischemia when given alone. The preconditioning-induced neuroprotection disappeared when 30 mg/kg 5HD was administered before test ischemia. These results suggest a possible involvement of adenosine A1 receptors during conditioning ischemia and of mitochondrial KATP channels during subsequent severe ischemia in the development of tolerance to focal cerebral ischemia.

scholarly journals Neuroprotective effect ofPanax ginsengextract against cerebral ischemia–reperfusion-injury-induced oxidative stress in middle cerebral artery occlusion models

FACETS ◽  
2019 ◽  
Vol 4 (1) ◽  
pp. 52-68 ◽  
Author(s):  
Mufzala Shamim ◽  
Nazish Iqbal Khan
Keyword(s):  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Lipid Profile ◽  
Liver Enzymes ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Liver And Kidney ◽  
Cerebral Artery Occlusion

The present study investigated the in vivo neuroprotective role of Panax ginseng extract (PGE) pretreatment against transient cerebral ischemia in a middle cerebral artery occlusion (MCAO) model. Rats were randomly divided as follows: group I, control; group II, sham-operated; group III, where animals were subjected to MCAO surgery; and group IV, where animals were orally administered 10 mL PGE per day (200 mg/kg of body weight per day) for 30 d followed by MCAO induction at day 31. Following 24 h of reperfusion, blood and tissue (brain, liver, and kidney) samples were collected for biochemical and histopathological examination. Biochemical testing included lipid profile, liver enzymes, kidney function tests, C-reactive protein (CRP), lactate dehydrogenase (LDH), glucose, and total protein estimation. Tissue antioxidants (catalase, superoxide dismutase, and glutathione) were assessed in brain, liver, and kidney tissues. MCAO-induced histopathological changes were also examined in the tissues. Pretreatment with PGE showed significant improvement in tissue antioxidant status in brain, liver and kidney tissues. PGE treatment maintains plasma lipid profile, liver enzymes, kidney function, and CRP, LDH, and glucose levels. Histologically, monocytes and macrophage infiltration were observed in the tissues of MCAO animals, whereas PGE treatment preserved tissue architecture and minimal monocyte infiltration. PGE supplementation showed a neuroprotective effect against ischemia–reperfusion injury by effectively increasing endogenous antioxidant enzyme activity.

The Neuroprotective Effect of Xenon Administration during Transient Middle Cerebral Artery Occlusion in Mice

2003 ◽  
Vol 99 (4) ◽  
pp. 876-881 ◽  
Author(s):  
H. Mayumi Homi ◽  
Noriko Yokoo ◽  
Daqing Ma ◽  
David S. Warner ◽  
Nicholas P. Franks ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
Cerebral Infarct ◽  
Cerebral Artery Occlusion

Background Xenon has been shown to be neuroprotective in several models of in vitro and in vivo neuronal injury. However, its putative neuroprotective properties have not been evaluated in focal cerebral ischemia. The purpose of this study was to determine if xenon offers neuroprotection in a mouse model of middle cerebral artery occlusion. Methods C57BL/6 mice underwent 60 min of middle cerebral artery occlusion. The animals (n = 21 per group) were randomized to receive either 70% xenon + 30% O2, 70% N2O + 30% O2, or 35% xenon + 35% N2O + 30% O2. After 24 h, functional neurologic outcome (on three independent scales: four-point, general, and focal deficit scales) and cerebral infarct size were evaluated. Results The 70% xenon + 30% O2 group showed improved functional outcome (median [interquartile range], four-point scale: 2 [2], 70% xenon + 30% O2 versus 3 [2], 70% N2O + 30% O2, P = 0.0061; general deficit scale: 9 [6], 70% xenon + 30% O2 versus 10 [4], 70% N2O + 30% O2, P = 0.0346). Total cerebral infarct volumes were reduced in the 70% xenon + 30% O2 group compared with the 70% N2O + 30% O2 group (45 +/- 17 mm3 versus 59 +/- 11 mm3, respectively; P = 0.0009). Conclusions In this model of transient focal cerebral ischemia, xenon administration improved both functional and histologic outcome.

Sign in / Sign up

Export Citation Format

Share Document