Miao Geng

Baicalin has shown multiple neuroprotective biological activities, including antiapoptotic and anti-inflammatory functions in neurodegeneration diseases. However, whether baicalin can regulate Aβ-induced microglial activation or inhibit inflammatory cytokine secretion has not been confirmed. We demonstrated that baicalin can inhibit beta amyloid peptides (Aβ42)-induced BV2 microglial cell proliferation, reduce the expression of CD11b, decrease chemotactic ability of BV2 cells and significantly inhibit the secretion of IL-6, TNF-α and NO. Moreover, baicalin pretreatment can effectively inhibit Aβ-induced phosphorylation of JAK2 and STAT3. Baicalin can inhibit Aβ-induced microglial cell activation by regulating the JAK2/STAT3 signaling pathway in AD transgenic mice. The modulation of microglial proliferation, activation and secretion by baicalin could be a promising therapeutic option for the treatment of Alzheimer's disease.

Aims. To further investigate the antineuroblastoma effect of rutin which is a type of flavonoid. Methods. The antiproliferation of rutin in human neuroblastoma cells LAN‐5 were detected by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay. Chemotaxis of LAN‐5 cells was assessed using transwell migration chambers and scratch wound migration assay. The cell cycle arrest and apoptosis in a dose‐dependent manner was measured by flow cytometric and fluorescent microscopy analyses. The apoptosis‐related proteins BAX and BCL2 as well as MYCN mRNA express were determined by RT‐PCR analysis. Secreted TNF‐α level were determined using specific enzyme‐linked immunosorbent assay kits. Results. Rutin significantly inhibited the growth of LAN‐5 cells and chemotactic ability. Flow cytometric analysis revealed that rutin induced G2/M arrest in the cell cycle progression and induced cell apoptosis. The RT‐PCR showed that rutin could decrease BCL2 expression and BCL2/BAX ratio. In the meantime, the MYCN mRNA level and the secretion of TNF‐α were inhibited. Conclusion. These results suggest that rutin produces obvious antineuroblastoma effects via induced G2/M arrest in the cell cycle progression and induced cell apoptosis as well as regulating the expression of gene related to apoptosis and so on. It supports the viability of developing rutin as a novel therapeutic prodrug for neuroblastoma treatment, as well as providing a new path on anticancer effect of Chinese traditional drug.