Abstract
The natural flavonoid glycoside baicalin (BA) produces a variety of pharmaceutical effects, particularly for psychiatric/neurological disorders. This study evaluated the behavioral and neuroprotective effects of BA in mice subjected to chronic unpredictable mild stress, a model of depression. BA (25 and 50 mg/kg) significantly increased sucrose consumption and reduced immobility times in the tail suspension and forced swim tests, demonstrating that BA alleviated depression-like behaviors. Moreover, BA reduced the levels of inflammatory cytokines, such as interleukin 1β, interleukin 6, and tumor necrosis factor α, in serum and in the hippocampus. BA also abrogated increases in NMDAR/NR2B and Ca2+/calmodulin-dependent protein kinase II, and the decrease in phosphorylated ERK and reactive oxygen species production in mice subjected to chronic unpredictable mild stress. These findings suggested that the antidepressive effects of BA are due to the regulation of an NMDAR/NR2B-ERK1/2-related pathway and inhibition of inflammatory cytokines and oxidative stress. Thus, BA represents a potential candidate drug for patients suffering from depression.
Highlights
Depression is a common mental disorder in which individuals experience bodily disturbances, loss of interest, and feelings of guilt, often leading to suicidal tendencies [1,2]
Mice subjected to chronic unpredictable mild stress (CUMS) were immobile for a longer time in the forced swimming test (FST) and TST than the control mice (Po0.01, n=8), whereas treatment with BA (25 and 50 mg/kg) and Flu (20 mg/kg) decreased the immobility times compared with control levels (Po0.01, n=8) (Figure 2B and C)
Effects of BA on proinflammatory cytokines Enzyme-linked immunosorbent assay (ELISA) revealed that CUMS increased the levels of IL
Summary
Depression is a common mental disorder in which individuals experience bodily disturbances (for example, out-of-tune embodiment and loss of bodily resonance), loss of interest, and feelings of guilt, often leading to suicidal tendencies [1,2]. Emerging evidence suggests that the pathological process of depression involves oxido-nitrosative stress and the neuroinflammatory cascade [4], as well as deficiencies in cell proliferation, aberrant cytokine production, and disordered neuroplasticity [5]. CUMS validly and reliably induces depression-like behaviors and physiological effects that mimic neuropsychiatric disorders [7,8]. The levels of various proinflammatory cytokines are increased in patients suffering from depression, and antiinflammatory therapy produces antidepressant effects in patients with autoimmune and inflammatory disorders [11,12]. These data have given rise to the hypothesis that the pathogenesis of major depression involves inflammatory processes and brain-systemic immune interactions
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