Interleukin-19 alleviates brain injury by anti-inflammatory effects in a mice model of focal cerebral ischemia

2016 ◽  
Vol 1650 ◽  
pp. 172-177 ◽  
Author(s):  
Weiying Xie ◽  
Lili Fang ◽  
Shuyuan Gan ◽  
Haojun Xuan
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Mice Model ◽  
Anti Inflammatory

The antioxidant effects of Joongpoongtang 05 on brain injury after transient focal cerebral ischemia in rats

2011 ◽  
Vol 65 (2) ◽  
pp. 322-329 ◽  
Author(s):  
Hyo Won Jung ◽  
Ramalingam Mahesh ◽  
Hyo Sang Bae ◽  
Young Ho Kim ◽  
Jong Seong Kang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Transient Focal Cerebral Ischemia ◽  
Antioxidant Effects

Aggravated chronic brain injury after focal cerebral ischemia in aquaporin-4-deficient mice

2012 ◽  
Vol 520 (1) ◽  
pp. 121-125 ◽  
Author(s):  
Wen-Zhen Shi ◽  
Ling-Ling Qi ◽  
San-Hua Fang ◽  
Yun-Bi Lu ◽  
Wei-Ping Zhang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Aquaporin 4 ◽  
Deficient Mice

Fentanyl Does Not Increase Brain Injury After Focal Cerebral Ischemia in Rats

1999 ◽  
Vol 88 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Vanna Soonthon-Brant ◽  
Piyush M. Patel ◽  
John C. Drummond ◽  
Daniel J. Cole ◽  
Paul J. Kelly ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia

scholarly journals Neuronal expression of the mitochondrial protein prohibitin confers profound neuroprotection in a mouse model of focal cerebral ischemia

2017 ◽  
Vol 38 (6) ◽  
pp. 1010-1020 ◽  
Author(s):  
Anja Kahl ◽  
Corey J Anderson ◽  
Liping Qian ◽  
Henning Voss ◽  
Giovanni Manfredi ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Mitochondrial Protein ◽  
Motor Impairment ◽  
Cell Types ◽  
Viral Gene ◽  
Sensory Motor ◽  
The Brain

The mitochondrial protein prohibitin (PHB) has emerged as an important modulator of neuronal survival in different injury modalities . We previously showed that viral gene transfer of PHB protects CA1 neurons from delayed neurodegeneration following transient forebrain ischemia through mitochondrial mechanisms. However, since PHB is present in all cell types, it is not known if its selective expression in neurons is protective, and if the protection occurs also in acute focal ischemic brain injury, the most common stroke type in humans. Therefore, we generated transgenic mice overexpressing human PHB1 specifically in neurons (PHB1 Tg). PHB1 Tg mice and littermate controls were subjected to transient middle cerebral artery occlusion (MCAo). Infarct volume and sensory-motor impairment were assessed three days later. Under the control of a neuronal promoter (CaMKIIα), PHB1 expression was increased by 50% in the forebrain and hippocampus in PHB1 Tg mice. The brain injury produced by MCAo was reduced by 63 ± 11% in PHB1 Tg mice compared to littermate controls. This reduction was associated with improved sensory-motor performance, suggesting that the salvaged brain remains functional. Approaches to enhance PHB expression may be useful to ameliorate the devastating impact of cerebral ischemia on the brain.

Role of AT1 receptors and NAD(P)H oxidase in diabetes-aggravated ischemic brain injury

2004 ◽  
Vol 286 (6) ◽  
pp. H2442-H2451 ◽  
Author(s):  
Ikuyo Kusaka ◽  
Gen Kusaka ◽  
Changman Zhou ◽  
Mami Ishikawa ◽  
Anil Nanda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Focal Cerebral Ischemia ◽  
Lipid Hydroperoxide ◽  
Neurological Deficits ◽  
Sprague Dawley

The objective of the present study was to examine the role of the angiotensin II type 1 receptor (AT1-R) in the diabetes-aggravated oxidative stress and brain injury observed in a rat model of combined diabetes and focal cerebral ischemia. Diabetes was induced by an injection of streptozotoxin (STZ; 55 mg/kg iv) at 8 wk of age. Two weeks after the induction of diabetes, some animals received continuous subcutaneous infusion of the AT1-R antagonist candesartan (0.5 mg·kg−1·day−1) for 14 days. Focal cerebral ischemia, induced by middle cerebral artery occlusion/reperfusion (MCAO), was conducted at 4 wk after STZ injection. Male Sprague-Dawley rats ( n = 189) were divided into five groups: normal control, diabetes, MCAO, diabetes + MCAO, and diabetes + MCAO + candesartan. The major observations were that 1) MCAO produced typical cerebral infarction and neurological deficits at 24 h that were accompanied by elevation of NAD(P)H oxidase gp91phox and p22phox mRNAs, and lipid hydroperoxide production in the ipsilateral hemisphere; 2) diabetes enhanced NAD(P)H oxidase gp91phox and p22phox mRNA expression, potentiated lipid peroxidation, aggravated neurological deficits, and enlarged cerebral infarction; and 3) candesartan reduced the expression of gp91phox and p22phox, decreased lipid peroxidation, lessened cerebral infarction, and improved the neurological outcome. We conclude that diabetes exaggerates the oxidative stress, NAD(P)H oxidase induction, and brain injury induced by focal cerebral ischemia. The diabetes-aggravated brain injury involves AT1-Rs. We have shown for the first time that candesartan reduces brain injury in a combined model of diabetes and cerebral ischemia.

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