Effect of baicalin on inflammatory response and TLR4/NF-κB signaling pathway of human brain microvascular endothelial cell after hypoxia-reoxygenation injury
【Abstract】In this study, the oxygen-glucose deprivation (OGD) model in the human brain microvascular endothelial cells (HBMECs) was used to simulate the ischemic neuronal damage, observe the inflammatory response, and explore the possible mechanisms for treating cerebral ischemia/reperfusion and improving memory impairment from the view point of inhibiting inflammatory response, which is of great reference significance for related Chinese medicine treatment of ischemic diseases. HBMECs were given with drugs at the same time of OGD injury, and reoxygenated for 2 h after treatment for 4 h. Cell supernatant was then collected, and the inflammatory factors in cell supernatant were detected. Immunofluorescence assay was used to detect HBMEC morphology and expression of p-nuclear factor kappa-light-chain-enhancer of activated B (p-NF-κB); Western blot was used to detect expression changes of Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MYD88) and p-NF-κB. The results showed that, after OGD modeling, the levels of interleukin 6 (IL-6), IL-1α, IL-1β and tumor necrosis factor-α (TNF-α) were significantly increased; baicalin protected HBMECs, inhibited intranuclear transcription of p-NF-κB, significantly decreased HBMEC release of inflammatory factors caused by OGD injury, and inhibited the expression of TLR4, MYD88, and p-NF-κB. The studies suggested that baicalin had obvious protective effect on HBMECs damaged by OGD, and could inhibit inflammatory response. Its protection mechanism may be related to inhibiting TLR4 signaling pathways.
【Keywords】 baicalin; human brain microvascular endothelial cell (HBMEC); cytokines; oxygen-glucose deprivation (OGD); TLR4; NF-κB;
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