FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2912108286> ?p ?o ?g. }

• W2912108286 endingPage "15" @default.
• W2912108286 startingPage "1" @default.
• W2912108286 abstract "Ischemic stroke is usually followed by inflammatory responses mediated by microglia. However, the effect of statins on directly preventing posthypoxia microglia inflammatory factors to prevent injury to surrounding healthy neurons is unclear. Atorvastatin and rosuvastatin, which have different physical properties regarding their lipid and water solubility, are the most common HMG-CoA reductase inhibitors (statins) and might directly block posthypoxia microglia inflammatory factors to prevent injury to surrounding neurons. Neuronal damage and microglial activation of the peri-infarct areas were investigated by Western blotting and immunofluorescence after 24 hours in a middle cerebral artery occlusion (MCAO) rat model. The decrease in neurons was in accordance with the increase in microglia, which could be reversed by both atorvastatin and rosuvastatin. The effects of statins on blocking secretions from posthypoxia microglia and reducing the secondary damage to surrounding normal neurons were studied in a coculture system in vitro . BV2 microglia were cultured under oxygen glucose deprivation (OGD) for 3 hours and then cocultured following reperfusion for 24 hours in the upper wells of transwell plates with primary neurons being cultured in the bottom wells. Inflammatory cytokines, including tumor necrosis factor- α (TNF- α ), interleukin-1 β (IL-1 β ), and cyclooxygenase-2 (COX2), which are activated by the nuclear factor-kappa B (NF- κ B) signaling pathway in OGD-induced BV2 microglia, promoted decreased release of the anti-inflammatory cytokine IL-10 and apoptosis of neurons in the coculture systems according to ELISA and Western blotting. However, pretreatment with atorvastatin or rosuvastatin significantly reduced neuronal death, synaptic injury, and amyloid-beta (A β ) accumulation, which might lead to increased low-density lipoprotein receptors (LDLRs) in BV2 microglia. We concluded that the proinflammatory mediators released from postischemia damage could cause damage to surrounding normal neurons, while HMG-CoA reductase inhibitors prevented neuronal apoptosis and synaptic injury by inactivating microglia through blocking the NF- κ B signaling pathway." @default.
• W2912108286 created "2019-02-21" @default.
• W2912108286 creator A5003564506 @default.
• W2912108286 creator A5010368680 @default.
• W2912108286 creator A5038680183 @default.
• W2912108286 creator A5042949590 @default.
• W2912108286 creator A5065574006 @default.
• W2912108286 creator A5075328429 @default.
• W2912108286 creator A5080001140 @default.
• W2912108286 creator A5083794006 @default.
• W2912108286 date "2019-02-17" @default.
• W2912108286 modified "2023-10-17" @default.
• W2912108286 title "HMG-CoA Reductase Inhibitors Attenuate Neuronal Damage by Suppressing Oxygen Glucose Deprivation-Induced Activated Microglial Cells" @default.
• W2912108286 cites W1492482999 @default.
• W2912108286 cites W1499442767 @default.
• W2912108286 cites W1606421883 @default.
• W2912108286 cites W1684804860 @default.
• W2912108286 cites W1781091308 @default.
• W2912108286 cites W1831632254 @default.
• W2912108286 cites W1965134490 @default.
• W2912108286 cites W1975572742 @default.
• W2912108286 cites W1988870129 @default.
• W2912108286 cites W1992571619 @default.
• W2912108286 cites W1999936371 @default.
• W2912108286 cites W2011860625 @default.
• W2912108286 cites W2012221575 @default.
• W2912108286 cites W2015426193 @default.
• W2912108286 cites W2028271379 @default.
• W2912108286 cites W2034845277 @default.
• W2912108286 cites W2035657272 @default.
• W2912108286 cites W2039550203 @default.
• W2912108286 cites W2053176712 @default.
• W2912108286 cites W2064080906 @default.
• W2912108286 cites W2083373599 @default.
• W2912108286 cites W2084744450 @default.
• W2912108286 cites W2085262263 @default.
• W2912108286 cites W2102308820 @default.
• W2912108286 cites W2112801385 @default.
• W2912108286 cites W2114052742 @default.
• W2912108286 cites W2116644918 @default.
• W2912108286 cites W2117978222 @default.
• W2912108286 cites W2118200665 @default.
• W2912108286 cites W2121581237 @default.
• W2912108286 cites W2121730272 @default.
• W2912108286 cites W2134137024 @default.
• W2912108286 cites W2139203136 @default.
• W2912108286 cites W2145291936 @default.
• W2912108286 cites W2158211941 @default.
• W2912108286 cites W2164795628 @default.
• W2912108286 cites W2171165037 @default.
• W2912108286 cites W2178290584 @default.
• W2912108286 cites W2189113876 @default.
• W2912108286 cites W2190256747 @default.
• W2912108286 cites W2269173565 @default.
• W2912108286 cites W2283674586 @default.
• W2912108286 cites W2308448653 @default.
• W2912108286 cites W2318735649 @default.
• W2912108286 cites W2322509087 @default.
• W2912108286 cites W2335436429 @default.
• W2912108286 cites W2436206117 @default.
• W2912108286 cites W2443300690 @default.
• W2912108286 cites W2480927613 @default.
• W2912108286 cites W2494842370 @default.
• W2912108286 cites W2507549382 @default.
• W2912108286 cites W2509510511 @default.
• W2912108286 cites W2515285024 @default.
• W2912108286 cites W2519134948 @default.
• W2912108286 cites W2527422074 @default.
• W2912108286 cites W2536113964 @default.
• W2912108286 cites W2592988020 @default.
• W2912108286 cites W2594853806 @default.
• W2912108286 cites W2595484157 @default.
• W2912108286 cites W2621131822 @default.
• W2912108286 cites W2754128384 @default.
• W2912108286 cites W2761635843 @default.
• W2912108286 cites W2762107040 @default.
• W2912108286 cites W2762154985 @default.
• W2912108286 cites W2768015798 @default.
• W2912108286 cites W2769635641 @default.
• W2912108286 cites W2790632213 @default.
• W2912108286 cites W2790844793 @default.
• W2912108286 cites W2793954020 @default.
• W2912108286 cites W2794855331 @default.
• W2912108286 cites W2801626566 @default.
• W2912108286 cites W2802131732 @default.
• W2912108286 cites W2804015886 @default.
• W2912108286 cites W2887121122 @default.
• W2912108286 doi "https://doi.org/10.1155/2019/7675496" @default.
• W2912108286 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6397982" @default.
• W2912108286 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30911291" @default.
• W2912108286 hasPublicationYear "2019" @default.
• W2912108286 type Work @default.
• W2912108286 sameAs 2912108286 @default.
• W2912108286 citedByCount "17" @default.
• W2912108286 countsByYear W29121082862019 @default.
• W2912108286 countsByYear W29121082862020 @default.
• W2912108286 countsByYear W29121082862021 @default.
• W2912108286 countsByYear W29121082862022 @default.

• next