Caffeic acid ameliorates early and delayed brain injuries after focal cerebral ischemia in rats

Zhou, Yu; Fang, San‐Hua; Ye, Yilu; Chu, Lisheng; Zhang, Weiping; Wang, Mengling; Wei, Er-qing

doi:10.1111/j.1745-7254.2006.00406.x

Cited by 67 publications

(54 citation statements)

References 34 publications

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“…For example, CAPE/caffeic acid has been reported to protect the brain against induced diabetes, quinolinic acid-induced brain damage, aluminuminduced toxicity, neonatal hypoxia, and transient focal ischemia (Celik and Erdogan, 2008;Kalonia et al, 2009;Khan et al, 2007;Wei et al, 2004;Yang et al, 2008;Zhou et al, 2006). Caffeic acid has also been reported to reduce lesion area and glial scar formation following cryoinjury in mice (Zhang et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Caffeic Acid Phenethyl Ester Protects Blood–Brain Barrier Integrity and Reduces Contusion Volume in Rodent Models of Traumatic Brain Injury

Zhao¹,

Pati

Redell³

et al. 2012

Journal of Neurotrauma

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A number of studies have established a deleterious role for inflammatory molecules and reactive oxygen species (ROS) in the pathology of traumatic brain injury (TBI). Caffeic acid phenethyl ester (CAPE) has been shown to exert both antioxidant and anti-inflammatory effects. The primary objective of the present study was to examine if CAPE could be used to reduce some of the pathological consequences of TBI using rodent models. Male Sprague-Dawley rats and C57BL/6 mice were subjected to controlled cortical impact (CCI) injury. Blood -brain barrier (BBB) integrity was assessed by examining claudin-5 expression and the extravasation of Evans blue dye. The effect of post-injury CAPE administration on neurobehavioral function was assessed using vestibulomotor, motor, and two hippocampus-dependent learning and memory tasks. We report that post-TBI administration of CAPE reduces Evans blue extravasation both in rats and mice. This improvement was associated with preservation of the levels of the tight junction protein claudin-5. CAPE treatment did not improve performance in either vestibulomotor/motor function (tested using beam balance and foot-fault tests), or in learning and memory function (tested using the Morris water maze and associative fear memory tasks). However, animals treated with CAPE were found to have significantly less cortical tissue loss than vehicle-treated controls. These findings suggest that CAPE may provide benefit in the treatment of vascular compromise following central nervous system injury.

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Section: Discussionmentioning

confidence: 99%

Caffeic Acid Phenethyl Ester Protects Blood–Brain Barrier Integrity and Reduces Contusion Volume in Rodent Models of Traumatic Brain Injury

Zhao¹,

Pati

Redell³

et al. 2012

Journal of Neurotrauma

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“…Ca 2ϩ is thought to facilitate binding of 5-LO to phosphatidylcholine on the nuclear membrane whereas ATP is thought to increase the 5-LO activity by stabilizing the protein structure through the C2-like domain (56). 5-LO inhibitors have been reported to improve cell survival, to protect against ischemia in vitro (61), and to be anti-inflammatory in vivo (74). The leukotrienes synthesized by 5-LO signal through at least two classes of G protein-coupled receptors, named cysteinyl leukotriene 1 (CysLT 1 ) and 2 (CysLT 2 ) receptors, which are widely expressed in cells of the immune system but in the case of CysLT 1 are also expressed in endothelial cells and the lung.…”

mentioning

confidence: 99%

Volume-sensitive release of organic osmolytes in the human lung epithelial cell line A549: role of the 5-lipoxygenase

Holm

Grygorczyk

Lambert

2013

American Journal of Physiology-Cell Physiology

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Holm JB, Grygorczyk R, Lambert IH. Volume-sensitive release of organic osmolytes in the human lung epithelial cell line A549: role of the 5-lipoxygenase. Am J Physiol Cell Physiol 305: C48-C60, 2013. First published March 13, 2013; doi:10.1152/ajpcell.00412.2012.-Pathophysiological conditions challenge cell volume homeostasis and perturb cell volume regulatory mechanisms leading to alterations of cell metabolism, active transepithelial transport, cell migration, and death. We report that inhibition of the 5-lipoxygenase (5-LO) with AA861 or ETH 615-139, the cysteinyl leukotriene 1 receptor (CysLT1) with the antiasthmatic drug Zafirlukast, or the volume-sensitive organic anion channel (VSOAC) with DIDS blocks the release of organic osmolytes (taurine, meAIB) and the concomitant cell volume restoration following hypoosmotic swelling of human type II-like lung epithelial cells (A549). Reactive oxygen species (ROS) are produced in A549 cells upon hypotonic cell swelling by a diphenylene iodonium-sensitive NADPH oxidase. The swelling-induced taurine release is suppressed by ROS scavenging (butylated hydroxytoluene, N-acetyl cysteine) and potentiated by H 2O2. Ca 2ϩ mobilization with ionomycin or ATP stimulates the swelling-induced taurine release whereas calmodulin inhibition (W7) inhibits the release. Chelation of the extracellular Ca 2ϩ (EGTA) had no effect on swelling-induced taurine release but prevented ATP-induced stimulation. H2O2, ATP, and ionomycin were unable to stimulate the taurine release in the presence of AA861 or Zafirlukast, placing 5-LO and CysLT1 as essential elements in the swelling-induced activation of VSOAC with ROS and Ca 2ϩ as potent modulators. Inhibition of tyrosine kinases (genistein, cucurbitacin) reduces volume-sensitive taurine release, adding tyrosine kinases (Janus kinase) as regulators of VSOAC activity. Caspase-3 activity during hypoxia is unaffected by inhibition of 5-LO/CysLT1 but reduced when swelling-induced taurine loss via VSOAC is prevented by DIDS excess extracellular taurine, indicating a beneficial role of taurine under hypoxia. 5-lipoxygenase; lung adenocarcinoma; cysteinyl leukotriene 1 receptor; hypoxia; ischemia; cell volume regulation; reactive oxygen species; taurine homeostasis WITHIN RECENT YEARS it has become clear that cell volume regulation under isotonic conditions and cell volume restoration following osmotic perturbations are important for regulation of the intracellular milieu and cellular functions, such as cell metabolism, cell migration, and control of cell death (see refs. 16, 39). Cells maintain a steady cell volume by regulating the intracellular concentrations of ions (mainly Na ϩ , K ϩ , and Cl Ϫ ) and organic osmolytes (16,39). A consequence of hypotonic cell swelling is net loss of KCl and amino acids including the ␤-amino ethane sulfonic acid, taurine.Taurine: a multifunctional amino acid. Taurine is the most abundant free amino acid of the human body and has been estimated to account for up to 38% of the total free amino acid pool in rat heart ce...

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“…Specifically, elevation of intracellular calcium that generally occurs after excitotoxicity and mitogen-activated protein kinase (MAPK)-regulated phosphorylation that can be induced by oxidative stress [3] both activate 5-LOX. Previously, we reported that 5-LOX can be activated after ischemic brain injury in rats [8,10] , after oxygen-glucose deprivation (OGD)-induced ischemic injury in cultured neurons and in pheochromocytoma (PC12) cells [11][12][13][14] . In primary neuron cultures, OGD induces release of excitatory amino acids that activate NMDA receptors to elevate intracellular calcium, resulting in 5-LOX translocation to the nuclear envelope and activation of 5-LOX to produce CysLTs [12] .…”

mentioning

confidence: 99%

“…5-LOX metabolites play an important role in inflammatory diseases of the peripheral tissues and the central nervous system, such as bronchial asthma [4,5] and ischemic brain injury [6][7][8][9] . In these diseases, various stimuli activate 5-LOX through two main ways.…”

mentioning

confidence: 99%

Baicalin attenuates oxygen-glucose deprivation-induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase activation in PC12 cells

Zhang

Fang

et al. 2010

Acta Pharmacol Sin

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Aim: To determine whether the flavonoid baicalin attenuates oxygen-glucose deprivation (OGD)-induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase (5-LOX) activation in PC12 cells. Methods: The effects of baicalin and the 5-LOX inhibitor zileuton on the changes induced by OGD/recovery or H 2 O 2 (an exogenous reactive oxygen species [ROS]) in green fluorescent protein-5-LOX-transfected PC12 cells were compared. Results: Both baicalin and zileuton attenuated OGD/recovery-and H 2 O 2 -induced injury and inhibited OGD/recovery-induced production of 5-LOX metabolites (cysteinyl leukotrienes) in a concentration-dependent manner. However, baicalin did not reduce baseline cysteinyl leukotriene levels. Baicalin also reduced OGD/recovery-induced ROS production and inhibited 5-LOX translocation to the nuclear envelope and p38 phosphorylation induced by OGD/recovery and H 2 O 2 . In contrast, zileuton did not show these effects. Conclusion: Baicalin can inhibit 5-LOX activation after ischemic injury, which may partly result from inhibition of the ROS/p38 mitogenactivated protein kinase pathway.

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Caffeic acid ameliorates early and delayed brain injuries after focal cerebral ischemia in rats

Cited by 67 publications

References 34 publications

Caffeic Acid Phenethyl Ester Protects Blood–Brain Barrier Integrity and Reduces Contusion Volume in Rodent Models of Traumatic Brain Injury

Caffeic Acid Phenethyl Ester Protects Blood–Brain Barrier Integrity and Reduces Contusion Volume in Rodent Models of Traumatic Brain Injury

Volume-sensitive release of organic osmolytes in the human lung epithelial cell line A549: role of the 5-lipoxygenase

Baicalin attenuates oxygen-glucose deprivation-induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase activation in PC12 cells

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