Аннотация:—A close relationship between the brain capillaries and the functional load of neurons andglial cells allows considering them as a single structural and functional complex, a neurovascularunit (NVU). The effects of lipopolysaccharide (LPS, 5–30 μg/mL, 24h) on nitric oxide (NO)production and of menadione (5–50 μM, 24 h) on cell viability in cultures of granule neurons,cerebrovascular endothelial cells and astrocytes, as well as the state of mitochondria (Mt) indifferent NVU cell types, were assessed. It was found that the application of 5 μg/mL of LPS causedan intense NO production in cell cultures. The largest effect was shown for astrocytes, in whichLPS caused a significant increase in NO production by more than 8 fold. In cultures of granuleneurons, this exposure caused an almost 5 fold increase in NO production. The weakest responseto the stimulation of NO production was shown for endotheliocytes, 1.7 fold. To induce oxidativedamage, menadione was introduced into a culture medium. In neuronal cultures, 10 μM ofmenadione was already enough to cause complete death of granule neurons. Damage toendotheliocytes and astrocytes was only observed when the menadione concentration increased upto 50 μM. Since menadione induced oxidative stress is mediated by mitochondria, the state of theMt was assessed in intact cells. In astrocytes and endotheliocytes, Mt were numerous andrepresented long curved strands, whereas in granule neurons, these organelles are much smaller insize and have a rounded shape. Thus, in the NVU, astrocytes are the main NO producers duringneuroinflammation, while neurons are the most sensitive to oxidative stress despite relatively poordevelopment of the mitochondrial network; cerebrovascular endothelial cells demonstrated aminimum contribution to NO production
