Dihydroartemisinin exerts cytotoxic effects and inhibits hypoxia inducible factor-1alpha activation in C6 glioma cells.

Artemisinin and its analogue dihydroartemisinin exert cytotoxic effects in some kinds of cancer cell lines. Here we determined whether dihydroartemisinin inhibits the growth and induces apoptosis of rat C6 glioma cells. We found dihydroartemisinin (5-25 microM) inhibited the growth and induced apoptosis of C6 cells in a concentration- and time-dependent manner; however, it was much less toxic to rat primary astrocytes.

[Dihydroartemisinin inhibits proliferation and induces apoptosis of rat glioma C6 cells].

Objective: To determine the effects of dihydroartemisinin (DHA) on the proliferation and apoptosis of rat glioma C6 cells.

Methods: DHA (1~ 125 micromol/L) was added into the cultured C6 cells and incubated for 24, 48 and 72 h. The cell proliferation and viability were determined by trypan blue exclusion assay and 3-(4, 5-dimethylthiazol-2yl)-2, 5 diphenyl tetrazolium bromide (MTT) reduction assay.

[Transfection with 5-lipoxygenase/green fluorescence protein for evaluating injury-induced 5-lipoxygenase translocation to the nuclear membrane in PC12 cells].

Objective: To evaluate the translocation of 5-lipoxygenase (5-LOX)) after injuries by transfection with green fluorescence protein (GFP)/5-LOX in PC12 cells.

Methods: PC12 cells were stably transfected with pEGFP-C2/5-LOX (GFP/5-LOX) or pEGFP-C2 vectors (control). After treatment with oxygen-glucose deprivation (OGD), H(2)O(2) or NMDA, GFP/5-LOX localization in the cells was observed under a fluorescence microscope.

Baicalin attenuates oxygen-glucose deprivation-induced injury via inhibiting NMDA receptor-mediated 5-lipoxygenase activation in rat cortical neurons.

The flavonoid baicalin exerts neuroprotective effects but the mechanism is not fully clarified. On the other hand, 5-lipoxygenase (5-LOX) activation is involved in ischemic neuronal injury. In this study, we determined whether baicalin protects rat cortical neurons against oxygen-glucose deprivation (OGD)-induced ischemic-like injury, if so, whether this effect relates to 5-LOX activation.

Activation of 5-lipoxygenase after oxygen-glucose deprivation is partly mediated via NMDA receptor in rat cortical neurons.

5-Lipoxygenase (5-LOX) is the enzyme metabolizing arachidonic acid to produce pro-inflammatory leukotrienes. We have reported that 5-LOX is translocated to the nuclear envelope after ischemic-like injury in PC12 cells. In the present study, we determined whether 5-LOX is activated (translocation and production of leukotrienes) after oxygen-glucose deprivation (OGD) in primary rat cortical neurons; if so, whether this activation is mediated by NMDA receptor.