Baicalin reverse depressive-like behaviors through regulation SIRT1-NF-kB signaling pathway in olfactory bulbectomized rats

Depression is a common and detrimental illness that affects up to 120 million people worldwide. The present study was designed to evaluate the antidepressant-like effects and mechanisms of baicalin on olfactory bulbectomized model of depression. Baicalin treatment (20 and 40 mg/kg) significantly reversed the abnormal levels of sucrose consumption, open field test, and forced swimming test. Treatments with baicalin reversed the olfactory bulbectomized-induced alterations of serum corticosterone levels to a great extent. Our results further demonstrated that baicalin administration negatively regulated the expression of interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF-alpha) in the hippocampus and hypothalamus. Furthermore, baicalin regulated Sirtuin 1 (SIRT1) and decreased the levels of p65 acetylation (ac-p65) in the hippocampus and hypothalamus. Moreover, in lipopolysaccharides-induced BV-2 cells, the levels of inflammatory factors (IL-1 beta), p65 acetylation at lysine 310, and SIRT1 expression were different in the group treated with both baicalin and nicotinamide compared with the group treated with baicalin, which suggests that baicalin regulates SIRT1 and thereby inhibits p65 acetylation. In summary, administration of baicalin reduces the levels of pro-inflammatory cytokines, possibly through regulation of SIRT1-NF-kB pathway. Our findings suggest a support into the potential of baicalin in therapeutic effect for depression.