Lu Liu
Henan University
13 Papers
41 Citations
Lu Liu is an academic researcher from Henan University. The author has contributed to research in topics: Blood–brain barrier & Medicine. The author has an hindex of 7, co-authored 11 publications.
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Papers
Alteration in P-glycoprotein at the blood-brain barrier in the early period of MCAO in rats.
TL;DR: The aim of this work was to investigate the alteration in P‐glycoprotein at the blood–brain barrier (BBB) after middle cerebral artery occlusion (MCAO) in rats.
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Modulation of P-glycoprotein in rat brain microvessel endothelial cells under oxygen glucose deprivation
TL;DR: To investigate modulation of P‐glycoprotein (P‐gp) in rat brain microvessel endothelial cells (rBMECs) under oxygen glucose deprivation (OGD), a new intracellular signalling molecule is introduced into the cell nucleus for the first time.
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HMGB1 promoted P-glycoprotein at the blood-brain barrier in MCAO rats via TLR4/NF-κB signaling pathway
TL;DR: HMGB1 promoted P-gp at the BBB after cerebral ischemia via TLR4/NF-κB signaling pathway, demonstrating that HMGB1 can release from nucleus to the cytoplasm in activated astrocytes, then into the medium.
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Anthraquinone derivative exerted hormetic effect on the apoptosis in oxygen-glucose deprivation-induced PC12 cells via ERK and Akt activated Nrf2/HO-1 signaling pathway
TL;DR: The results suggested that the effect of BME on the OGD-induced PC12 cells may be hormetic mechanism including induction of oxidative stress and subsequent activation of stress response gene expression.
21
Polyamine analogue QMA attenuated ischemic injury in MCAO rats via ERK and Akt activated Nrf2/HO-1 signaling pathway.
TL;DR: Treatment with QMA attenuated ischemic damage accompanying up regulation of Nuclear factor erythroid 2‐related factor, Heme oxygenase‐1 (HO‐1), p‐ERK and p‐Akt in cerebral cortex tissues of middle cerebral artery occlusion rats and oxygen‐glucose deprivation (OGD)‐treated PC12 cells suggested that the protective actions of QMA may be related to activation of endogenous cytoprotective mechanism via ERK and Ak
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