Targeting Caveolin-1 as a Therapeutic Approach to Prevent Blood-Brain Barrier Breakdown in Ischemic Stroke
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Home > Medicine & Health Science textbooks > Medicine: general issues > Targeting Caveolin-1 as a Therapeutic Approach to Prevent Blood-Brain Barrier Breakdown in Ischemic Stroke: From Mechanism to Isoflavones Treatment
Targeting Caveolin-1 as a Therapeutic Approach to Prevent Blood-Brain Barrier Breakdown in Ischemic Stroke: From Mechanism to Isoflavones Treatment

Targeting Caveolin-1 as a Therapeutic Approach to Prevent Blood-Brain Barrier Breakdown in Ischemic Stroke: From Mechanism to Isoflavones Treatment


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About the Book

This dissertation, "Targeting Caveolin-1 as a Therapeutic Approach to Prevent Blood-brain Barrier Breakdown in Ischemic Stroke: From Mechanism to Isoflavones Treatment" by Yong, Gu, 顧勇, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Our group previously reported that caveolin-1 (cav-1) was down-regulated by nitric oxide (NO) during cerebral ischemia and reperfusion (I/R). However, the role of cav-1 in regulating blood-brain barrier (BBB) permeability is unclear yet. This study aims to address whether the loss of cav-1 induced by NO production affects BBB permeability. Data showed that the expression of cav-1 in isolated cortical microvessels was down-regulated in ischemia-reperfused rat brains subjected to middle cerebral artery occlusion (MCAO). Treatment of NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, reserved cav-1 expression, inhibited matrix metalloproteinases (MMPs) activity and reduced the BBB permeability. Moreover, cav-1 knockdown remarkably increased MMPs activity in the culture medium of brain microvascular endothelial cells. Cav-1 deficiency mice displayed higher MMPs activity and BBB permeability than that of the wild-type mice. Interestingly, the effects of L-NAME on MMPs activity and BBB permeability were partly reversed in cav-1 deficiency mice. These results suggest that cav-1 plays important roles in regulating MMPs activity and BBB permeability in cerebral I/R injury. After completing the mechanism study, I investigated the potential drug candidate that targets cav-1 for protecting BBB and neuronal damage during cerebral I/R. Results showed that calycosin, an isoflavones from Astragali Radix, up-regulated the expression of cav-1 and inhibited MMPs activity, and decreased the BBB permeability in the MCAO ischemia-reperfused rat brains. I further investigated the neuroprotective effects of isoflavones of Astragali Radix, with in vitro oxygen glucose deprivation (OGD) model and in vivo cerebral ischemia-reperfusion models. In addition to calycosin and formononetin, two major isoflavones in Astragali Radix, daidzein was also included because it is a metabolite of formononetin after absorption. Results showed that all three isoflavones decreased infarction volume and neurological scores in MCAO rats and dose-dependently attenuated neuronal death induced by L-glutamate treatment and oxygen-glucose deprivation plus reoxygenation (OGD/RO). The neuroprotective effects were inhibited by estrogen receptors (ER) antagonist ICI 182,780. Interestingly, combine treatment of isoflavones displayed synergistic effects in both OGD/RO and L-glutamate induced neuronal injury models, as well as in MCAO cerebral ischemia-reperfusion rat brains. Mechanistically, estrogen receptor antagonist partly reduced the synergism in these models. PI3K/Akt activation was synergistically induced by treatment of those isoflavones simultaneously. In summary, cav-1 could be a potential therapeutic target for protecting the BBB in the treatment of cerebral I/R injury. Major findings in this thesis include: 1) Cav-1 plays an important role in maintaining BBB integrity through inhibition of MMPs activity. NO induced MMPs activities and BBB leakage are partially mediated by the down-regulation of cav-1 during cerebral I/R injury. 2) Calycosin treatment reserved cav-1 expression and reduced BBB permeability. 3) Isoflavones synergistically protected neurons against I/R-induced neuronal insults both in vitro and in vivo. The works provide a valuable step towards the clarification of the physiological and pathophysiological functions of c


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Product Details
  • ISBN-13: 9781361341421
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 220
  • Sub Title: From Mechanism to Isoflavones Treatment
  • Width: 216 mm
  • ISBN-10: 1361341424
  • Publisher Date: 26 Jan 2017
  • Binding: Hardback
  • Language: English
  • Spine Width: 14 mm
  • Weight: 803 gr


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Targeting Caveolin-1 as a Therapeutic Approach to Prevent Blood-Brain Barrier Breakdown in Ischemic Stroke: From Mechanism to Isoflavones Treatment
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Targeting Caveolin-1 as a Therapeutic Approach to Prevent Blood-Brain Barrier Breakdown in Ischemic Stroke: From Mechanism to Isoflavones Treatment
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