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Bilobalide alleviates neuroinflammation and promotes autophagy in Alzheimer's disease by upregulating lincRNA-p21.

EGb 761 has some protective effects on AD and can improve the cognitive functions of AD mice. However, the underlying molecular mechanisms are unknown. Here, we investigated the function of bilobalide, the effective component of EGb 761, in neuroinflammation and autophagy during AD. LPS-treated BV-2 cells were used as an in vitro model for neuroinflammation. The APP/PS1 AD mouse line was used to examine the function of bilobalide in AD. ELISA and qRT-PCR were used to measure the levels of proinflammatory cytokines, including TNF-α, IL-6 and IL-1β. Western blotting was employed to determine the protein levels of p-p65, iNOS, COX-2, LC3, beclin-1, p62 and p-STAT3. Immunostaining was applied to examine the number of autophagosomes. LPS treatment induced inflammatory responses and inhibited autophagy in BV-2 cells. Bilobalide suppressed LPS-induced neuroinflammation and promoted autophagy. Furthermore, bilobalide treatment increased the lincRNA-p21 levels, which suppressed STAT3 signalling. Knockdown of lincRNA-p21 reversed the effects of bilobalide. Overexpression of lincRNA-p21 promoted autophagy and inhibited neuroinflammation as well while STAT3 inhibitor blocked the effects of si-lincRNA-p21. In vivo experiments revealed that bilobalide improved the learning and memory capabilities of APP/PS1 AD mice. Bilobalide improves the cognitive functions of APP/PS1 AD mice. Mechanistically, bilobalide suppresses inflammatory responses and promotes autophagy possibly by upregulating lincRNA-p21 levels.