Role of MC-1 alone and in combination with tissue plasminogen activator in focal ischemic brain injury in rats

2005 ◽  
Vol 103 (1) ◽  
pp. 165-169 ◽  
Author(s):  
Chen Xu Wang ◽  
Tao Yang ◽  
Raza Noor ◽  
Ashfaq Shuaib
Keyword(s):  
Brain Injury ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Tissue Plasminogen

Tissue-plasminogen activator-induced ischemic brain injury is reversed by melatonin: role of iNOS and Akt

2005 ◽  
Vol 39 (2) ◽  
pp. 151-155 ◽  
Author(s):  
Ertugrul Kilic ◽  
Ülkan Kilic ◽  
Russel J. Reiter ◽  
Claudio L. Bassetti ◽  
Dirk M. Hermann
Keyword(s):  
Brain Injury ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Tissue Plasminogen

Abstract WMP99: Alpha2-Antiplasmin Inactivation Reduces Hemorrhagic Transformation and Ischemic Brain Injury After Tissue Plasminogen Activator Therapy and Mechanical Reperfusion

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Sofiyan Saleem ◽  
Guy L Reed
Keyword(s):  
Brain Injury ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Infarct Volume ◽  
Ischemic Brain Injury ◽  
Brain Hemorrhage ◽  
Brain Swelling ◽  
Brain Infarct ◽  
Ischemic Brain ◽  
Tissue Plasminogen

Tissue plasminogen activator (r-tPA) therapy followed by thrombectomy-mediated, mechanical reperfusion profoundly reduces neurologic disability in appropriately selected patients. Nevertheless, a high proportion of these patients (20-37%) develop brain hemorrhage. We examined the contribution of α2-antiplasmin, a fast-acting plasmin inhibitor, to brain hemorrhage and ischemic injury following r-tPA treatment and mechanical reperfusion. Methods: Mice (C57Bl6) underwent 1 to 4 h of middle cerebral artery occlusion followed by treatment with r-tPA alone (10 mg/kg), r-tPA (10 mg/kg) plus an α2AP inhibitor (α2AP-I, 10 mg/kg) antibody or saline, followed by reperfusion. Mice were assessed by neurobehavioral measures (Bederson score and corner test) and histology 24 h post-ischemic stroke. Analyses were performed in a blinded fashion. Time course studies in r-tPA-treated mice showed that intracerebral hemorrhage (p<0.05), brain infarct volume (p<0.001) and brain swelling (p<0.01) increased progressively with ischemic time, with a plateau at 3 h of ischemia, as compared to saline treated controls. Mice treated at 3 h with r r-tPA + α2AP-I showed significantly (p<0.05) reduced brain hemorrhage, brain infarct volume (p<0.01) and brain swelling (p<0.05). Treatment with r-tPA + α2AP-I also significantly improved neurobehavioral deficits (p<0.01) and sensory motor dysfunction (p<0.01) at 24h of reperfusion. Conclusion: α2AP contributes to the increased brain hemorrhage and ischemic brain injury associated with r-tPA treatment followed by mechanical reperfusion. Targeting a2AP appears beneficial, because specific, monoclonal antibody-mediated inhibition of α2AP markedly reduced brain hemorrhage, infarction, swelling and neurobehavioral disability.

scholarly journals Rosiglitazone Alone Or in Combination with Tissue Plasminogen Activator Improves Ischemic Brain Injury in an Embolic Model in Rats

2009 ◽  
Vol 29 (10) ◽  
pp. 1683-1694 ◽  
Author(s):  
Chen Xu Wang ◽  
Xiuqing Ding ◽  
Raza Noor ◽  
Christina Pegg ◽  
Chunyan He ◽  
...  
Keyword(s):  
Brain Injury ◽  
Plasminogen Activator ◽  
Collagen Type ◽  
Collagen Type Iv ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Type Iv ◽  
Injured Brain ◽  
Tissue Plasminogen ◽  
Rosiglitazone Treatment

In this study, we examined whether rosiglitazone, a peroxisome proliferator-activated receptor gamma (PPAR γ) agonist, is neuroprotective in focal ischemic brain injury, and whether rosiglitazone can enhance the protective action of tissue plasminogen activator (tPA), an agent used clinically for thrombolytic therapy. Rats were subjected to ischemic brain injury by embolizing preformed clots into the middle cerebral artery (MCA). Treatment with rosiglitazone reduced infarction and improved functional recovery; it also enhanced the neuroprotective action of tPA and lengthened the time window for initiating tPA treatment. Occlusion of MCA resulted in a loss of collagen type IV, a major structural protein of the microvascular basal lamina, and tPA treatment worsened this loss. Rosiglitazone treatment prevented the reduction of collagen type IV in the ischemic injured brain by inhibiting the activation of matrix metallopeptidase-9 (MMP-9). In addition, rosiglitazone treatment reduced inflammatory reactions in the ischemic injured brain. Rosiglitazone either alone or in combination with tPA is an effective agent in the reduction of ischemic brain injury. The reduction of microvascular damage and inflammation contributes to the beneficial actions of rosiglitazone.

scholarly journals Role of P225 and the C136-C201 disulfide bond in tissue plasminogen activator

1998 ◽  
Vol 7 (8) ◽  
pp. 1728-1737 ◽  
Author(s):  
Alessandro Vindigni ◽  
Enrico Di Cera
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Disulfide Bond ◽  
Tissue Plasminogen

scholarly journals Effects of sevoflurane on rats with ischemic brain injury and the role of the TREK-1 channel

2017 ◽  
Vol 14 (4) ◽  
pp. 2937-2942 ◽  
Author(s):  
Lixiao Pan ◽  
Fengyun Yang ◽  
Caixia Lu ◽  
Changxin Jia ◽  
Qing Wang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain
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