PubMed · 9577251
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1998. Quercetin.. https://pubmed.ncbi.nlm.nih.gov/9577251/
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The objective of this study is to determine the biological effects of various antiadhesion agents on macrophages, which play an essential role in wound healing and adhesion. To determine these effects, RAW264.7 macrophages were activated with lipopolysaccharide in the presence of antiadhesion agents: oxidized regenerated cellulose (oxyC), sodium hyaluronate (HA), dexamethasone (Dex), or chondroitin sulfate (CS). The release of nitric oxide (NO), vascular endothelial growth factor (VEGF), interleukin-6 (IL-6), or matrix metalloproteinases (MMPs) from RAW264.7 was measured. We found that oxyC reduced the release of NO, IL-6, MMP-2, and MMP-9, whereas it enhanced the release of VEGF. HA reduced the release of MMP-2, whereas it enhanced the release of VEGF and NO. HA exhibited no significant effect on the release of IL-6 or MMP-9. Dex reduced the release of NO, VEGF, IL-6, MMP-2, and MMP-9. CS reduced the release of VEGF, IL-6, and MMP-2, although it had no significant effect on the release of NO and MMP-9. Antiadhesion agents, which have been clinically used as physical barriers, modulated the functions of macrophages.
BACKGROUND: There is evidence that, even during remission, schizophrenia (SZ) patients are especially vulnerable to de-compensate under stress, and that they tend to have a high baseline serum cortisol levels. This study was undertaken to determine whether raising serum cortisol by the infusion of hydrocortisone, in the absence of additional psychological stress, would result in different cerebral activity changes in schizophrenic patients compared to normal controls (CON). We were especially interested in cerebral activity in regions such as the medial temporal lobe and hippocampus, since structural abnormalities in these brain regions were frequent in association with schizophrenia. METHODS: Serum cortisol levels were raised, by infusing hydrocortisone, in 8 pairwise-matched SZ patients and 8 CONs. The associated regional cerebral activity changes were analyzed using statistical parametric mapping (SPM). RESULTS: There was increased regional cerebral activity in response to elevated cortisol in the left hippocampal region in the SZ group, while the controls showed evidence of decreased regional cerebral activity in the same anatomical location. For the rest of the brain regions, cerebral activity increases and decreases, in response to raised serum cortisol, in the SZ followed the same regional pattern as in the control group, but with a smaller overall magnitude of change. The blunted response in SZ was most marked in the regions that showed greatest regional cerebral activity changes in normal subjects. CONCLUSION: Patients with schizophrenia showed an abnormal increased regional cerebral activity response to cortisol infusion in the left hippocampal region, and similar but attenuated regional cerebral activity response in other regions, when compared to matched controls.
Vascular endothelial growth factor (VEGF) is a potent and specific mitogen for vascular endothelial cells. To examine whether platelet-activating factor (PAF) induces the expression of VEGF in human astrocytes, we stimulated cultured normal astrocytes with PAF and performed semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) or real-time quantitative PCR for VEGF mRNA and enzyme-linked immunosorbent assay for VEGF protein. PAF increased the expression of VEGF in astrocytes in time- and dose-dependent manners. After 24-h stimulation, 10 nM PAF increased the levels of VEGF protein in astrocyte-conditioned medium by 1.3-fold. When the cells were subjected to hypoxia, the PAF-induced production of VEGF was enhanced by 6.7-fold as compared to the unstimulated cells incubated under normoxia. Dexamethasone was found to inhibit the enhanced VEGF production in response to the stimulation with PAF under hypoxia. We conclude that PAF induces VEGF gene expression in human astrocytes, and the PAF-induced increase in the expression of VEGF may modulate nervous tissue injury due to hypoxia.