Neuroprotective effect of curcumin on focal cerebral ischemic rats by preventing blood–brain barrier damage

Jiang, Jun; Wang, Wei; Sun, Yong; Mei, Hu; Li, Fēi; Zhu, Dong Ya

doi:10.1016/j.ejphar.2006.12.028

Cited by 191 publications

(127 citation statements)

References 36 publications

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“…38 Exogenous peroxynitrite has been shown to mediate BBB permeabilization in an ECV304/C6 coculture model and in vivo. 39,40 Because NO release as well has been demonstrated to be involved in BBB disruption (for review, see Thiel and Audus 41 ), we examined whether CRP affects endothelial NO synthesis and whether this has an effect on the CRP-induced loss of barrier function. In the present experiments, CRP neither affected intracellular NO formation nor did blockade of the NO synthase prevent CRP-induced BBB disruption.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of C-Reactive Protein-Induced Blood–Brain Barrier Disruption

Kuhlmann

Librizzi

Closhen³

et al. 2009

Stroke

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Background and Purpose-Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood-brain barrier stability and to analyze the underlying signaling pathways. Methods-We used a cell coculture model of the blood-brain barrier and the guinea pig isolated whole brain preparation. Results-We could show that CRP at clinically relevant concentrations (10 to 20 g/mL) causes a disruption of the blood-brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fc␥ receptors CD16/32 followed by p38-mitogen-activated protein kinase-dependent reactive oxygen species formation by the NAD(P)H-oxidase. The resulting oxidative stress increased myosin light chain kinase activity leading to an activation of the contractile machinery. Blocking myosin light chain phosphorylation prevented the CRP-induced blood-brain barrier breakdown and the disruption of tight junctions. Conclusions-Our data identify a previously unrecognized mechanism linking CRP and brain edema formation and present a signaling pathway that offers new sites of therapeutic intervention.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of C-Reactive Protein-Induced Blood–Brain Barrier Disruption

Kuhlmann

Librizzi

Closhen³

et al. 2009

Stroke

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“…below) mediate curcumin's neuroprotective effect in ischemic stroke models . Several reports also suggest that curcumin preserves the integrity of the blood-brain barrier under ischemic conditions (Jiang et al, 2007;Kaur and Ling, 2008;Wang et al, 2013).…”

Section: A Ischemia: Stroke and Myocardial Infarctionmentioning

confidence: 99%

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

et al. 2014

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“…Evidence indicates that curcumin may act as a neuroprotective substance on postischemic outcome and behavioral deficits in rodents and this neuroprotective effect is presented by antiapoptotic action [66,74,75]. Other studies have shown that curcumin reverses the permeability of the ischemic blood-brain barrier and decreases brain edema [13,20]. Additionally in behavioral studies in rodents curcumin reverses cognitive changes [13].…”

Section: Potent Neuroprotective Activity Of Curcuminmentioning

confidence: 99%