The Experts below are selected from a list of 1425 Experts worldwide ranked by ideXlab platform

Sylvain Doré - One of the best experts on this subject based on the ideXlab platform.

  • Prostaglandin D_2 DP1 receptor is beneficial in ischemic stroke and in acute exicitotoxicity in young and old mice
    AGE, 2010
    Co-Authors: Abdullah Shafique Ahmad, Muzamil Ahmad, Takayuki Maruyama, Shuh Narumiya, Sylvain Doré
    Abstract:

    The cardiovascular complications reported to be associated with cyclooxygenase inhibitor use have shifted our focus toward prostaglandins and their respective receptors. Prostaglandin D_2 and its DP1 receptor have been implicated in various normal and pathologic conditions, but their role in stroke is still poorly defined. Here, we tested whether DP1 deletion aggravates N -methyl- d -aspartic acid (NMDA)-induced acute toxicity and whether DP1 pharmacologic activation protects mice from acute excitotoxicity and transient cerebral ischemia. Moreover, since the elderly are more vulnerable to stroke-related damage than are younger patients, we tested the susceptibility of aged DP1 knockout (DP1^−/−) mice to Brain damage. We found that intrastriatal injection of 15 nmol NMDA caused significantly larger lesion volumes (27.2 ± 6.4%) in young adult DP1^−/− mice than in their wild-type counterparts. Additionally, intracerebroventricular pretreatment of wild-type mice with 10, 25, and 50 nmol of the DP1-selective agonist BW245C significantly attenuated the NMDA-induced lesion Size by 19.5 ± 5.0%, 39.6 ± 7.7%, and 28.9 ± 7.0%, respectively. The lowest tested dose of BW245C also was able to reduce middle cerebral artery occlusion-induced Brain Infarction Size significantly (21.0 ± 5.7%). Interestingly, the aggravated NMDA-induced Brain damage was persistent in older DP1^−/− mice as well. We conclude that the DP1 receptor plays an important role in attenuating Brain damage and that selective targeting of this receptor could be considered as an adjunct therapeutic tool to minimize stroke damage.

  • Prostaglandin D2 DP1 receptor is beneficial in ischemic stroke and in acute exicitotoxicity in young and old mice
    Age, 2010
    Co-Authors: Abdullah Shafique Ahmad, Muzamil Ahmad, Takayuki Maruyama, Shuh Narumiya, Sylvain Doré
    Abstract:

    The cardiovascular complications reported to be associated with cyclooxygenase inhibitor use have shifted our focus toward prostaglandins and their respective receptors. Prostaglandin D2 and its DP1 receptor have been implicated in various normal and pathologic conditions, but their role in stroke is still poorly defined. Here, we tested whether DP1 deletion aggravates N-methyl-d-aspartic acid (NMDA)-induced acute toxicity and whether DP1 pharmacologic activation protects mice from acute excitotoxicity and transient cerebral ischemia. Moreover, since the elderly are more vulnerable to stroke-related damage than are younger patients, we tested the susceptibility of aged DP1 knockout (DP1−/−) mice to Brain damage. We found that intrastriatal injection of 15 nmol NMDA caused significantly larger lesion volumes (27.2 ± 6.4%) in young adult DP1−/− mice than in their wild-type counterparts. Additionally, intracerebroventricular pretreatment of wild-type mice with 10, 25, and 50 nmol of the DP1-selective agonist BW245C significantly attenuated the NMDA-induced lesion Size by 19.5 ± 5.0%, 39.6 ± 7.7%, and 28.9 ± 7.0%, respectively. The lowest tested dose of BW245C also was able to reduce middle cerebral artery occlusion-induced Brain Infarction Size significantly (21.0 ± 5.7%). Interestingly, the aggravated NMDA-induced Brain damage was persistent in older DP1−/− mice as well. We conclude that the DP1 receptor plays an important role in attenuating Brain damage and that selective targeting of this receptor could be considered as an adjunct therapeutic tool to minimize stroke damage.

Milan Basta - One of the best experts on this subject based on the ideXlab platform.

  • Combination Therapy with Low-Dose IVIG and a C1-esterase Inhibitor Ameliorates Brain Damage and Functional Deficits in Experimental Ischemic Stroke
    NeuroMolecular Medicine, 2018
    Co-Authors: Xinzhi Chen, Thiruma V. Arumugam, Yi-lin Cheng, Jong-hwan Lee, Srinivasulu Chigurupati, Mark P. Mattson, Milan Basta
    Abstract:

    Acute ischemic stroke causes a high rate of deaths and permanent neurological deficits in survivors. Current interventional treatment, in the form of enzymatic thrombolysis, benefits only a small percentage of patients. Brain ischemia triggers mobilization of innate immunity, specifically the complement system and Toll-like receptors (TLRs), ultimately leading to an exaggerated inflammatory response. Here we demonstrate that intravenous immunoglobulin (IVIG), a scavenger of potentially harmful complement fragments, and C1-esterase inhibitor (C1-INH), an inhibitor of complement activation, exert a beneficial effect on the outcome of experimental Brain ischemia (I) and reperfusion (R) injury induced by transient occlusion of middle cerebral artery in mice. Both IVIG and C1-INH significantly and in a dose–responsive manner reduced Brain Infarction Size, neurological deficit and mortality when administered to male mice 30 min before ischemia or up to 6 h after the onset of reperfusion. When combined, suboptimal doses of IVIG and C1-INH potentiated each other’s neuroprotective therapeutic effects. Complement C3 and TLR2 signals were colocalized and significantly greater in Brain cells adjacent to infracted Brain lesions when compared to the corresponding regions of the contralateral hemisphere and to control (sham) mice. Treatment with IVIG and C1-INH effectively reduced deposition of C3b and downregulated excessive TLR2 and p-JNK1 expression at the site of I/R injury. Taken together, these results provide a rationale for potential use of IVIG and C1-INH, alone or in combination with ischemic stroke and other neurological conditions that involve inappropriately activated components of the innate immune system.

  • High-dose intravenous immunoglobulin exerts neuroprotective effect in the rat model of neonatal asphyxia
    Pediatric Research, 2014
    Co-Authors: Bo Chen, Jeong Seon Yoon, Milan Basta
    Abstract:

    Background: Neonatal asphyxia is one of the leading causes of death in newborn and permanent neurological disabilities in surviving children. The underlying hypoxic-ischemic (HI) injury triggers an inflammatory response lading to neuronal damage. Here, we tested the hypothesis that high-dose intravenous immunoglobulin (IVIG) could exert immunomodulatory effect in rat pups subjected to HI injury. Methods: HI injury was induced in 7-d-old pups by ligating the common carotid artery followed by exposure to 8% oxygen for 2 h. Brain Infarction was evaluated by imaging stained coronal Brain sections. Neurological deficits were assessed in weeks 1 through 4 after HI. Western blotting and immunohistochemistry were used to assess complement fragment deposition in the Brain tissue. Results: Treatment with IVIG at 2 g/kg significantly and in a dose-responsive manner reduced Brain Infarction Size as well as mortality and neurological deficits caused by HI. Anatomical and functional improvements in IVIG-treated pups correlated with decreased deposition of C3b complement fragments in the injured Brain hemisphere. Conclusion: IVIG significantly improved the outcome of HI injury in rat pups and could potentially be used for the treatment of human neonatal asphyxia to target proinflammatory complement fragments.

Abdullah Shafique Ahmad - One of the best experts on this subject based on the ideXlab platform.

  • Prostaglandin D_2 DP1 receptor is beneficial in ischemic stroke and in acute exicitotoxicity in young and old mice
    AGE, 2010
    Co-Authors: Abdullah Shafique Ahmad, Muzamil Ahmad, Takayuki Maruyama, Shuh Narumiya, Sylvain Doré
    Abstract:

    The cardiovascular complications reported to be associated with cyclooxygenase inhibitor use have shifted our focus toward prostaglandins and their respective receptors. Prostaglandin D_2 and its DP1 receptor have been implicated in various normal and pathologic conditions, but their role in stroke is still poorly defined. Here, we tested whether DP1 deletion aggravates N -methyl- d -aspartic acid (NMDA)-induced acute toxicity and whether DP1 pharmacologic activation protects mice from acute excitotoxicity and transient cerebral ischemia. Moreover, since the elderly are more vulnerable to stroke-related damage than are younger patients, we tested the susceptibility of aged DP1 knockout (DP1^−/−) mice to Brain damage. We found that intrastriatal injection of 15 nmol NMDA caused significantly larger lesion volumes (27.2 ± 6.4%) in young adult DP1^−/− mice than in their wild-type counterparts. Additionally, intracerebroventricular pretreatment of wild-type mice with 10, 25, and 50 nmol of the DP1-selective agonist BW245C significantly attenuated the NMDA-induced lesion Size by 19.5 ± 5.0%, 39.6 ± 7.7%, and 28.9 ± 7.0%, respectively. The lowest tested dose of BW245C also was able to reduce middle cerebral artery occlusion-induced Brain Infarction Size significantly (21.0 ± 5.7%). Interestingly, the aggravated NMDA-induced Brain damage was persistent in older DP1^−/− mice as well. We conclude that the DP1 receptor plays an important role in attenuating Brain damage and that selective targeting of this receptor could be considered as an adjunct therapeutic tool to minimize stroke damage.

  • Prostaglandin D2 DP1 receptor is beneficial in ischemic stroke and in acute exicitotoxicity in young and old mice
    Age, 2010
    Co-Authors: Abdullah Shafique Ahmad, Muzamil Ahmad, Takayuki Maruyama, Shuh Narumiya, Sylvain Doré
    Abstract:

    The cardiovascular complications reported to be associated with cyclooxygenase inhibitor use have shifted our focus toward prostaglandins and their respective receptors. Prostaglandin D2 and its DP1 receptor have been implicated in various normal and pathologic conditions, but their role in stroke is still poorly defined. Here, we tested whether DP1 deletion aggravates N-methyl-d-aspartic acid (NMDA)-induced acute toxicity and whether DP1 pharmacologic activation protects mice from acute excitotoxicity and transient cerebral ischemia. Moreover, since the elderly are more vulnerable to stroke-related damage than are younger patients, we tested the susceptibility of aged DP1 knockout (DP1−/−) mice to Brain damage. We found that intrastriatal injection of 15 nmol NMDA caused significantly larger lesion volumes (27.2 ± 6.4%) in young adult DP1−/− mice than in their wild-type counterparts. Additionally, intracerebroventricular pretreatment of wild-type mice with 10, 25, and 50 nmol of the DP1-selective agonist BW245C significantly attenuated the NMDA-induced lesion Size by 19.5 ± 5.0%, 39.6 ± 7.7%, and 28.9 ± 7.0%, respectively. The lowest tested dose of BW245C also was able to reduce middle cerebral artery occlusion-induced Brain Infarction Size significantly (21.0 ± 5.7%). Interestingly, the aggravated NMDA-induced Brain damage was persistent in older DP1−/− mice as well. We conclude that the DP1 receptor plays an important role in attenuating Brain damage and that selective targeting of this receptor could be considered as an adjunct therapeutic tool to minimize stroke damage.

Shudong Wang - One of the best experts on this subject based on the ideXlab platform.

  • Neuroprotective effect of parthenocissin A, a natural antioxidant and free radical scavenger, in focal cerebral ischemia of rats.
    Phytotherapy research : PTR, 2010
    Co-Authors: Jiehong Yang, Yuanjiang Pan, Haitong Wan, Yu Wang, Shudong Wang
    Abstract:

    Neuroprotective effects of parthenocissin A (PA), a novel antioxidant and free radical scavenger, were studied in a transient middle cerebral artery (MCA) occlusion model in rats for the first time. The animals were treated intraperitoneally with PA at 2.5, 5 or 10 mg/kg, for both 30 min before MCA occlusion and 6 h after reperfusion. The MCA was occluded for 1 h in anesthetized Sprague-Dawley rats. Compared with vehicle-treated controls, MCA occluded animals treated with PA showed dose-dependent reductions in Brain Infarction Size with improved neurological and motor outcome. Biomedical assay showed that the PA treatment suppressed lipid peroxidation and restored superoxide dismutase (SOD) activity in Brain tissue. In addition, the ischemia/reperfusion (I/R) induced elevation of nitric oxide (NO) production and nitric oxide synthase (NOS) activity in Brain tissue was also inhibited. Thus, PA demonstrated a neuroprotective effect in the I/R model and the beneficial effects of the compound may result from the reduction of oxidative stress and the inhibition of NO production induced by I/R. The neuroprotective effects of PA have highlighted the potential use of stilbene oligomers in stroke therapy.

  • Neuroprotective effect of parthenocissin A, a natural antioxidant and free radical scavenger, in focal cerebral ischemia of rats.
    Phytotherapy Research, 2009
    Co-Authors: Jiehong Yang, Yuanjiang Pan, Haitong Wan, Yu Wang, Shudong Wang
    Abstract:

    Neuroprotective effects of parthenocissin A (PA), a novel antioxidant and free radical scavenger, were studied in a transient middle cerebral artery (MCA) occlusion model in rats for the first time. The animals were treated intraperitoneally with PA at 2.5, 5 or 10 mg/kg, for both 30 min before MCA occlusion and 6 h after reperfusion. The MCA was occluded for 1 h in anesthetized Sprague-Dawley rats. Compared with vehicle-treated controls, MCA occluded animals treated with PA showed dose-dependent reductions in Brain Infarction Size with improved neurological and motor outcome. Biomedical assay showed that the PA treatment suppressed lipid peroxidation and restored superoxide dismutase (SOD) activity in Brain tissue. In addition, the ischemia/reperfusion (I/R) induced elevation of nitric oxide (NO) production and nitric oxide synthase (NOS) activity in Brain tissue was also inhibited. Thus, PA demonstrated a neuroprotective effect in the I/R model and the beneficial effects of the compound may result from the reduction of oxidative stress and the inhibition of NO production induced by I/R. The neuroprotective effects of PA have highlighted the potential use of stilbene oligomers in stroke therapy. Copyright © 2009 John Wiley & Sons, Ltd.

Chen Xin-hua - One of the best experts on this subject based on the ideXlab platform.

  • Effect of Panax notoginseng saponins on MMP-9 expression after focal cerebral ischemia-reperfusion
    2004
    Co-Authors: Chen Xin-hua
    Abstract:

    Objective To investigate the effect of Panax notoginseng saponins on metalloproteinase-9 ( MMP-9 ) expression after focal cerebral ischemia-reperfusion. -Methods Using intravascular thread model with 2 h occlusion and 22 h reperfusion in rats, the Brain Infarction Size and the degree of blood-Brain barrier ( BBB) disruption in the ischemic region were evaluated. MMP-9 expression was evaluated by semi-quantitative RT-PCR. Results The Brain Infarction volume and area of BBB disruption were dramatically decreased in treatment group as compared to control group. The level of MMP-9 mRNA in experimental group was significantly lower than control rats. Conclusion BBB disruption and ischemic injury were attenuated by Panax notoginseng saponins after focal cerebral ischemia-reperfusion, one mechanism is through its inhibition of MMP-9 expression.