2016
DOI: 10.1016/j.brainres.2016.04.038
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D-allose protects the blood brain barrier through PPARγ-mediated anti-inflammatory pathway in the mice model of ischemia reperfusion injury

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Cited by 33 publications
(21 citation statements)
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“…Among others, D-Allose is the most active compound in MECN, reported to inhibit mitochondrial reactive oxygen species in Neuro2A cells [ 32 ] as well as protect the brain from transient ischemic neural death [ 33 ]. During cerebral ischemia, this compound also inhibited the production of inflammatory cytokines and translocation of NF-κB components to protect blood-brain barrier [ 34 , 35 ]. Phytol was found to produce significant anxiolytic activity in mice which is mediated through its interaction with GABAergic system [ 36 ].…”
Section: Discussionmentioning
confidence: 99%
“…Among others, D-Allose is the most active compound in MECN, reported to inhibit mitochondrial reactive oxygen species in Neuro2A cells [ 32 ] as well as protect the brain from transient ischemic neural death [ 33 ]. During cerebral ischemia, this compound also inhibited the production of inflammatory cytokines and translocation of NF-κB components to protect blood-brain barrier [ 34 , 35 ]. Phytol was found to produce significant anxiolytic activity in mice which is mediated through its interaction with GABAergic system [ 36 ].…”
Section: Discussionmentioning
confidence: 99%
“…*** P < 0.001, ** P < 0.01 vs. Control; ### P < 0.001, ## P < 0.01 vs. IR;^^^P < 0.001,^^P < 0.01 vs. D-allose (Shinohara et al 2016). Moreover, Huang, T. et al noticed that the blood brain barrier could be protected by D-allose via mediating anti-inflammatory pathway when I/R injury occurred in mice (Huang et al 1642). Given that, D-allose was proved to be negative to the releasing of inflammatory factors.…”
Section: Discussionmentioning
confidence: 99%
“…In various experimental models of arthritis, PPAR-γ activation has been shown to exhibit an anti-inflammatory effect and reduce the severity of the disease [ 33 , 34 ]. Apart from its direct genomic effect, PPAR-γ has been found to interact negatively with other transcription factors such as NF-κB, which underlies many aspects of the anti-inflammatory effect of PPAR-γ [ 35 , 36 ]. Many reports have documented that activated PPAR-γ can inhibited NF-κB signaling pathways to protect against RA [ 37 , 38 ].…”
Section: Discussionmentioning
confidence: 99%