2016
DOI: 10.1016/j.brainres.2016.08.012
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Senkyunolide I attenuates oxygen-glucose deprivation/reoxygenation-induced inflammation in microglial cells

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Cited by 34 publications
(16 citation statements)
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“…Moreover, stachydrine, leonurine, ferulic acid and Z -ligustilide might mediate the expressions of F2, HIF1α, and EPOR to improve blood circulation, thus exerting the effects of immune enhancement, erythrocyte synthesis and blood-vessel dilation ( Bi et al, 2012 ). Senkyunolide I may interact with MAPK1, IL-1β, and TNF-α, which were also involved in anemia and vascular systems ( Hu et al, 2016 ).…”
Section: Resultsmentioning
confidence: 99%
“…Moreover, stachydrine, leonurine, ferulic acid and Z -ligustilide might mediate the expressions of F2, HIF1α, and EPOR to improve blood circulation, thus exerting the effects of immune enhancement, erythrocyte synthesis and blood-vessel dilation ( Bi et al, 2012 ). Senkyunolide I may interact with MAPK1, IL-1β, and TNF-α, which were also involved in anemia and vascular systems ( Hu et al, 2016 ).…”
Section: Resultsmentioning
confidence: 99%
“…In recent studies, LC has been shown to possess anti-inflammatory properties via suppression of proinflammatory cytokines [ 25 , 29 ]. Usually, lipopolysaccharides (LPS) act as an endotoxin to induce the production of many proinflammatory cytokines in both in vitro and in vivo assays to study the anti-inflammatory properties of an active component.…”
Section: Molecular Mechanisms Of Lc's Anti-inflammatory Antioxidamentioning
confidence: 99%
“…In a study by Mahmoud et al, ferulic acid has been found to block the NF- κ B pathway which is activated by ROS [ 47 ]. Moreover, Hu et al proposed that senkyunolide I, another bioactive compound in LC, is able to reduce the ROS-induced production of TNF- α , IL-1 β , IL-6, and IFN- γ in BV-2 cells [ 29 ].…”
Section: Molecular Mechanisms Of Lc's Anti-inflammatory Antioxidamentioning
confidence: 99%
“…For instance, ERK5 activity seems to be protective while ERK1/2, c-Jun N-terminal kinase (JNK), and p38 may add to brain damage by increasing inflammation. [ 27 28 29 30 31 32 33 ] Accordingly, inhibition of ERK1/2, JNK, and p38 has been shown to decrease brain inflammation and improve functional recovery. [ 34 35 36 37 ] Stimulation of ERK1/2 pathway, however, may also paradoxically reduce injury by blocking apoptosis and release of trophic factors after global brain ischemia.…”
Section: Pathophysiology Of Brain Injury After Cardiac Arrestmentioning
confidence: 99%