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improved PIA-induced depressive-like behavior but not anxiety-like behavior in adult mice. Astrocytes play an essential role in regulating neuroinflammation, and are the most abundant cell type in the brain. In the PIA model, we found that ASB selectively inhibited astrocyte activation but not microglial activation in the cortex 

and hippocampus. Moreover, our results showed that ASB specifically upregulated the expression of menin protein in astrocytes and blocked the entry of P65 protein into the nucleus, thus inhibiting the secretion of IL-1β and TNF-α by astrocytes. Taken together, ASB reduced the occurrence of astrocyte-mediated neuroinflammation by targeting menin, thereby attenuating the PIA-induced depressive-like behavior. Our results reveal that ASB may be an attractive antidepressant drug and exert an antidepressant effect in PIA. In terms of drug selection, ASB may be a specific drug for patients with depressive symptoms.

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2.2. Experimental design for drug treatment

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The experimental design and drug treatment schedule are shown in Fig. 1A. The experimental animals were randomly divided into three groups: control, PIA, and PIA+ASB. ASB (DESITE, Chengdu, China)was dissolved in 1% DMSO and diluted with saline. For the PIA+ASB group, LPS and ASB (4 mg/kg/day) were administered intraperitoneally from P3 for 3 days. 

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