Abstract

Elevated inflammation is commonly observed in depression, but whether this association is causal is not determined. Our previous basic research indicated that Dl-3-n-butylphthalide (NBP) possessed an anti-inflammatory effect. Additional recent evidence consistently suggests that depression is associated with lipid metabolism. Therefore, our study performed an untargeted lipidomics approach of ultra-performance liquid chromatography coupled with mass spectrometry (UPLC-MS) to reveal the potential discriminating lipid profile of the hippocampus for NBP involvement in lipopolysaccharide (LPS)-induced depression. Male Sprague-Dawley(SD) rats were randomly allocated to one of three groups (n = 6): control, LPS-induced model of depression (LPS), or NBP involvement in the LPS-induced model of depression (LPS + NBP). Statistical analysis was used to identify differential hippocampus lipids in the LPS, NBP + LPS, and control groups. Our study demonstrated that most of the differentially expressed lipid metabolites were involved in glycerophospholipid metabolism, sphingolipid metabolism, glycerolipid metabolism, and glycosylphosphatidylinositol(GPI)-anchor biosynthesis, which may partially account for the pathophysiological process of depression. However, more pre-clinical and clinical evidence is warranted to determine the extent and consistency of the role of NBP and further elucidate the pathophysiological mechanisms underlying inflammation-induced depression.

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