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Bbb reperfusion

Wei Cai, Kai Zhang, Peiying Li, Ling Zhu, Jing Xu, Boyu Yang, Xiaoming Hu, Zhengqi Lu, Jun Chen
Current understanding on the mechanisms of brain injury and neurodegeneration highlights an appreciation of multicellular interactions within the neurovascular unit (NVU), which include the evolution of blood-brain barrier (BBB) damage, neuronal cell death or degeneration, glial reaction, and immune cell infiltration. Aging is an important factor that influences the integrity of the NVU. The age-related physiological or pathological changes in the cellular components of the NVU have been shown to increase the vulnerability of the NVU to ischemia/reperfusion injury or neurodegeneration, and to result in deteriorated brain damage...
September 30, 2016: Ageing Research Reviews
Rongrong Zhang, Mengxue Xu, Yu Wang, Fei Xie, Gang Zhang, Xinyue Qin
Stroke is one of the leading causes of death and disability in the world. Oxidative stress, which refers to an excessive generation of reactive oxygen species (ROS), plays a key role in the pathological process of stroke. Excessive ROS production contributes to brain ischemia/reperfusion injury through many mechanisms including BBB disruption, inflammation, apoptosis, and cellular necrosis. Nuclear factor-E2-related factor 2 (Nrf2) is one of the critical regulators of endogenous antioxidant defense, which promote the transcription of a wide variety of antioxidant genes...
September 30, 2016: Molecular Neurobiology
Alireza Partoazar, Sanaz Nasoohi, Sayed Mehdi Rezayat, Kambiz Gilani, Shahram Ejtemaei Mehr, Amir Amani, Nastaran Rahimi, Ahmad Reza Dehpour
Cyclosporin A (CsA) is known as a neuroprotective agent against cerebral ischemia/reperfusion (I/R) in animal models. However, the significant therapeutic effects of CsA have been observed in high systemic doses or manipulating the blood brain barrier (BBB), resulting in systemic side effects and toxicity. Since the liposome nanocarries have been developed for efficient delivery of peptide and proteins, liposomal CsA (Lipo-CsA) could improve cerebral (I/R) injuries. In this study, the liposomal CsA formulation (CsA at dose of 2...
September 12, 2016: Fundamental & Clinical Pharmacology
Mei-Yin Chien, Cheng-Hung Chuang, Chang-Ming Chern, Kou-Tong Liou, Der-Zen Liu, Yu-Chang Hou, Yuh-Chiang Shen
Salvianolic acid A (SalA), a chemical type of caffeic acid trimer, has drawn great attention for its potent bioactivities against ischemia-induced injury both in vitro and in vivo. In this study, we evaluated SalA's protective effects against acute ischemic stroke by inducing middle cerebral artery occlusion/reperfusion (MCAO) injuries in mice. Treatment of the mice with SalA (50 and 100μg/kg, i.v.) at 2h after MCAO enhanced their survival rate, improved their moving activity, and ameliorated the severity of brain infarction and apoptosis seen in the mice by diminishing pathological changes such as the extensive breakdown of the blood-brain barrier (BBB), nitrosative stress, and the activation of an inflammatory transcriptional factor p65 nuclear factor-kappa B (NF-κB) and a pro-apoptotic kinase p25/Cdk5...
September 5, 2016: Free Radical Biology & Medicine
Guosheng Cao, Nan Jiang, Yang Hu, Yuanyuan Zhang, Guangyun Wang, Mingzhu Yin, Xiaonan Ma, Kecheng Zhou, Jin Qi, Boyang Yu, Junping Kou
Ruscogenin, an important steroid sapogenin derived from Ophiopogon japonicus, has been shown to inhibit cerebral ischemic injury. However, its potential molecular action on blood-brain barrier (BBB) dysfunction after stroke remains unclear. This study aimed to investigate the effects of ruscogenin on BBB dysfunction and the underlying mechanisms in middle cerebral artery occlusion/reperfusion (MCAO/R)-injured mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-injured mouse brain microvascular endothelial cells (bEnd...
2016: International Journal of Molecular Sciences
Eun Soo Kim, Seung-Koo Lee, Mi Jung Kwon, Phil Hye Lee, Young-Su Ju, Dae Young Yoon, Hye Jeong Kim, Kwan Seop Lee
OBJECTIVE: The purpose of this study was to evaluate the effects of localized brain cooling on blood-brain barrier (BBB) permeability following transient middle cerebral artery occlusion (tMCAO) in rats, by using dynamic contrast-enhanced (DCE)-MRI. MATERIALS AND METHODS: Thirty rats were divided into 3 groups of 10 rats each: control group, localized cold-saline (20℃) infusion group, and localized warm-saline (37℃) infusion group. The left middle cerebral artery (MCA) was occluded for 1 hour in anesthetized rats, followed by 3 hours of reperfusion...
September 2016: Korean Journal of Radiology: Official Journal of the Korean Radiological Society
Joon Ha Park, Ki-Yeon Yoo, In Hye Kim, Jeong-Hwi Cho, Jae-Chul Lee, Ji Hyeon Ahn, Hyun Jin Tae, Bing Chun Yan, Dae Won Kim, Ok Kyu Park, Seung-Hae Kwon, Song Her, Jin Su Kim, Jung Hoon Choi, Choong Hyun Lee, In Koo Hwang, Jae Youl Cho, Jun Hwi Cho, Young-Guen Kwon, Sungwoo Ryoo, Young-Myeong Kim, Moo-Ho Won, Il Jun Kang
Hydroquinone (HQ), a major benzene metabolite, occurs naturally in various plants and is manufactured for commercial use. Although HQ displays various biological effects, its neuroprotective effects following ischemic insults have not been investigated. In this study, we first examined neuroprotective effects of HQ in a rat model of transient focal cerebral ischemia. Animals were subjected to transient middle cerebral artery occlusion for 120 min. HQ (50 or 100 mg/kg) or vehicle was intraperitoneally administered once at 30 min after ischemia-reperfusion...
August 31, 2016: Toxicological Sciences: An Official Journal of the Society of Toxicology
Fangzhe Chen, Weifeng Wang, Hongyan Ding, Qi Yang, Qiang Dong, Mei Cui
BACKGROUND: As the number of patients with cardioembolic ischemic stroke is predicted to be double by 2030, increased burden of warfarin-associated hemorrhagic transformation (HT) after cerebral ischemia is an expected consequence. However, thus far, no effective treatment strategy is available for HT prevention in routine clinical practice. While the glucagon-like peptide-1 receptor (GLP-1R) agonist exendin-4 (Ex-4) is known to protect against oxidative stress and neuronal cell death caused by ischemic brain damage, its effect on preventing warfarin-associated HT after cerebral ischemia is yet unknown...
2016: Journal of Neuroinflammation
Sajjad Muhammad, Oliver Planz, Markus Schwaninger
BACKGROUND: Thrombolysis is the only approved therapy for acute stroke. However, life-threatening complications such as intracerebral hemorrhage (ICH) can develop after intravenous administration of tissue plasminogen activator (tPA). Both infection and thrombolysis during cerebral ischemia disrupt the blood-brain barrier (BBB). tPA can induce matrix metalloproteinase-9 (MMP-9), which is known to be involved in BBB disruption. However, it has still not been investigated whether preexisting influenza virus infection during thrombolysis after acute stroke affects systemic levels of MMP-9 and its inhibitor TIMP-1 and whether increased systemic MMP-9 levels affect ICH...
2016: Cerebrovascular Diseases Extra
Shiyao Liu, Yanwei Yang, Mu Jin, Siyu Hou, Xiuhua Dong, Jiakai Lu, Weiping Cheng
Previous studies have shown that xenon-delayed postconditioning for up to 2h after reperfusion provides protection against spinal cord ischemia/reperfusion (I/R) injury in rats. This study was designed to determine the roles of phosphatidylinositol 3-kinase (PI3K)-Akt and extracellular signal-regulated kinase (ERK) in this neuroprotection. The rats were randomly assigned to the following nine groups (n=16∗9): 1) I/R+N2 group, 2) I/R+Xe group, 3) I/R+PD98059+N2 group (ERK blocking agent), 4) I/R+wortmannin+N2 group (PI3K-Akt blocking agent), 5) I/R+PD98059+Xe group, 6) I/R+wortmannin+Xe group, 7) I/R+DMSO+Xe group (dimethyl sulfoxide, vehicle control), 8) I/R+DMSO+N2 group, and 9) sham group (no spinal cord ischemia and no xenon)...
September 15, 2016: Journal of the Neurological Sciences
Burak Kazanci, Selcuk Ozdogan, Ramazan Kahveci, Emre Cemal Gokce, Kazim Yigitkanli, Aysun Gokce, Bulent Erdogan
AIM: We aimed in this study to evaluate the effect of pregabalin pretreatment on spinal cord ischemia-reperfusion(I/R) injury and compare it with methylprednisolone(MP). MATERIAL AND METHODS: Rats were randomized into four groups as follow: group 1 (sham)(n=8), group 2 (ischemia only)(n=8), group 3 (30 mg/kg pregabalin)(n=8), and group 4 (30 mg/kg methylprednisolone)(n=8). Laparotomy was performed without aortic clamp in the sham group. All animals were killed at 24 h after surgery...
April 27, 2016: Turkish Neurosurgery
Alexis N Simpkins, Christian Dias, Richard Leigh
BACKGROUND AND PURPOSE: Animal models of acute cerebral ischemia have demonstrated that diffuse blood-brain barrier (BBB) disruption can be reversible after early reperfusion. However, irreversible, focal BBB disruption in humans is associated with hemorrhagic transformation in patients receiving intravenous thrombolytic therapy. The goal of this study was to use a magnetic resonance imaging biomarker of BBB permeability to differentiate these 2 forms of BBB disruption. METHODS: Acute stroke patients imaged with magnetic resonance imaging before, 2 hours after, and 24 hours after treatment with intravenous tissue-type plasminogen activator were included...
September 2016: Stroke; a Journal of Cerebral Circulation
Ziyan Zhang, Jingqi Yan, Honglian Shi
Diabetes is a major stroke risk factor and is associated with poor functional recovery after stroke. Accumulating evidence indicates that the worsened outcomes may be due to hyperglycemia-induced cerebral vascular complications, especially disruption of the blood-brain barrier (BBB). The present study tested a hypothesis that the activation of hypoxia inducible factor-1 (HIF-1) was involved in hyperglycemia-aggravated BBB disruption in an ischemic stroke model. Non-diabetic control and Streptozotocin-induced type I diabetic mice were subjected to 90min transient middle cerebral artery occlusion (MCAO) followed by reperfusion...
November 2016: Neurobiology of Disease
S-H Xu, M-S Yin, B Liu, M-L Chen, G-W He, P-P Zhou, Y-J Cui, D Yang, Y-L Wu
Disruption of blood-brain barrier (BBB) and subsequent oedema are major causes of the pathogenesis in ischaemic stroke with which the current clinical therapy remains unsatisfied. In this study, we examined the therapeutic effect of tetramethylpyrazine-2'-O-sodium ferulate (TSF)-a novel analogue of tetramethylpyrazine in alleviating BBB breakdown and brain oedema after cerebral ischaemia/reperfusion (I/R). Then, we explored the potential mechanism of the protection on BBB disruption in cerebral I/R rat models...
July 6, 2016: Human & Experimental Toxicology
Firoozeh Alavian, Sohrab Hajizadeh, Mohammad Reza Bigdeli, Mohammad Javan
Recent studies suggest that normobaric hyperoxia (HO) protects the rat brain from ischemia reperfusion (IR) injury. Protein kinase C (PKC) is a key signaling molecule involved in protection against IR injury but its role in protective effect of HO in brain injury in unknown. In this study we attempted to see if PKC is involved in the effect of HO. Rats were divided into four main experimental groups. The first two were exposed to 95 % oxygen (HO) in a chamber 4 h/day for 6 consecutive days. Each of these groups had a control group exposed to 21 % oxygen...
2012: EXCLI journal
Abhishek Mukherjee, Sibani Sarkar, Snehasikta Swarnakar, Nirmalendu Das
Recent evidences suggest that cerebral ischemia-reperfusion insult plays significant role in pathogenic diseases like Alzheimer's disease (AD) and other neurodegenerative diseases. Toxic reactive oxygen species (ROS) generated by induced oxidative stress in the episodes of cerebral ischemia-reperfusion (CIR) acted as the main role in neurodegeneration. As the prime source of ROS generation, neuronal mitochondria which is the cellular energy metabolic centre experience severe damage because of CIR-induced oxidative stress...
June 24, 2016: Current Alzheimer Research
Haijun Bao, Xiaofang Yang, YuXiu Huang, Haiyang Qiu, Genping Huang, Hua Xiao, Jinxia Kuai
Adipocytokine apelin-13 is a peptide which could reportedly protect the brain against ischemic reperfusion injury and traumatic brain injury (TBI). Whether apelin-13 has any roles to play in intracerebral hemorrhage (ICH) has not been clarified. We aimed to investigate the roles of apelin-13 in ICH and effects on ICH-induced apoptosis. Firstly, CD-1 mice were subjected to infusion of Type IV collagenase (to induce ICH) or saline (for shams) into the left striatum. ICH animals received intracerebroventricular administration of vehicle, apelin-13 (50μg dissolved in 5μl saline) immediately after ICH...
August 15, 2016: Neuroscience Letters
Han-Sen Chen, Su-Hua Qi, Jian-Gang Shen
Tissue plasminogen activator (t-PA) is the only FDA approved drug for acute ischemic stroke treatment, but its clinical use is limited due to the narrow therapeutic time window and severe adverse effects, including hemorrhagic transformation (HT) and neurotoxicity. One of the potential resolutions is to use adjunct therapies to reduce the side effects and extend t-PA's therapeutic time window. However, therapies modulating single target seems not satisfying, and a multi-target strategy is warranted to resolve such complex disease...
June 19, 2016: Current Neuropharmacology
Dan Lu, Yan Qu, Fei Shi, Dayun Feng, Kai Tao, Guodong Gao, Shiming He, Tianzhi Zhao
G protein-coupled estrogen receptor 1 (GPER-1) plays important roles in estrogen-mediated neuroprotection. However, protective effects of GPER-1 on blood-brain barrier (BBB) after ischemic stroke have not been determined. The aim of present study was to determine whether GPER-1 activation ameliorates BBB permeability in ovariectomized rats with induced global cerebral ischemia (GCI). GCI was induced by 4-vessel occlusion for 20 min followed by 24 h reperfusion period. The GPER-1 agonist (G1) was bilaterally administered immediately upon reperfusion by intracerebroventricular (icv) injection...
August 19, 2016: Biochemical and Biophysical Research Communications
Ling-Lei Kong, Zhi-Yuan Wang, Jin-Feng Hu, Yu-He Yuan, Hua Li, Nai-Hong Chen
Disruption of blood-brain barrier (BBB) and subsequent edema are major contributors to the pathogenesis of ischemic stroke, and the current clinical therapy remains unsatisfied. Chemokine-like factor 1 (CKLF1), as a novel C-C chemokine, plays important roles in immune response. The expression of CKLF1 increased after focal cerebral ischemia and inhibition of CKLF1 activity showed neuroprotective effect by alleviating infiltration of neutrophil and neuron apoptosis in cerebral ischemia. However, few studies have focused on the role of CKLF1 on BBB integrity...
August 3, 2016: Neuroscience Letters
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