[Effects of Xuesaitong injection on inflammation induced by OGD/reoxygenation in BV2 microglia].

The present study aims to investigate the effects of Xuesaitong (XST)injection on inflammation induced by OGD/reoxygenation in BV2 microglia cell and explore the underlying mechanisms.The effects of XST injection were evaluated in terms of cell viability, secretion of TNF-α, IL-1ß, IL-6 and IL-10 into culture media, protein expression of p-ERK1/2, p-JNK and p-p38, and nuclear translocation of NF-κB p65. The results showed that XST injection significantly increased cell viability, suppressed release of TNF-α, IL-1ß, IL-6 and IL-10 and down-regulated p-JNK1/2 and p-p38 MAPK expression in BV2 microglia cells induced by OGD/R injury, whereas it had no effect on p-ERK1/2 expression. Furthermore, XST injection suppressed nuclear translocation of NF-κB p65 in BV2 microglia after OGD/R injury. These data indicate that the neuroprotective effects of XST injection on OGD/R injury are associated with its inhibition of pro-inflammatory mediator production, down-regulation of JNK1/2 and p38 MAPK activation, and suppression of NF-κB p65 nuclear translocation in BV2 microglia cells.

Knockdown of E2F3 Inhibits Proliferation, Migration, and Invasion and Increases Apoptosis in Glioma Cells.

E2F3a, as a member of the E2F family, is essential for cell division associated with the progression of many cancers. However, the biological effect of E2F3a on glioma is not understood as well. To investigate the functional mechanism of E2F3a in glioma, we examined the expression of E2F3a in glioma tissue and cell lines. We found that E2F3a was upregulated in glioma tissue compared with adjacent tissue, and this was associated with a poor survival rate. E2F3a was highly expressed in glioma cell lines compared with normal HEB cell lines. Knockdown of E2F3a significantly inhibited cell proliferation, promoted G0/G1 phase arrest, elevated apoptosis rates, and suppressed cell migration and invasion. However, overexpression of E2F3a markedly promoted cell proliferation, migration, and invasion and inhibited apoptosis. Moreover, in vivo studies showed that knockdown of E2F3a expression dramatically inhibited U373 tumor growth in a nude mouse model. Results of real-time PCR and Western blot showed that the depletion of E2F3a upregulated the expression levels of cell apoptosis-related proteins and downregulated migration-related proteins. Conversely, E2F3a overexpression downregulated the expression levels of cell apoptosis-related proteins and upregulated migration-related proteins. In conclusion, our results highlight the importance of E2F3a in glioma and provide new insights into the diagnostics and therapeutics of gliomas.