Abstract
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.
This work was supported by the National Natural Science Foundation (Grant no. 81041206) of China and the Traditional Medicine Special Project of PLA of China (Grant no. 10ZYZ244).