Baicalin Attenuates Continuous Activation of β-Catenin Induced by Lipopolysaccharide (LPS) and Depression Complicated by Infertility in Male Rats

Abstract

Background. Baicalin (BA) is a potential candidate drug to inhibit depressive behavior. However, the mechanism of BA's role on depression complicated with male infertility (DCMI) is still unclear. This study aimed to investigate the role of BA in alleviating inflammatory factor-induced DCMI by regulating β-catenin. Methods. Firstly, we performed sucrose preference test (SPT), open field test (OFT), tail suspension test (TST), and forced swim test (FST) in the chronic unpredictable mild stress (CUMS) + lipopolysaccharide (LPS) model rats to study the effect of BA on depressive behavior. The levels of neuropeptide Y (NPY), testosterone (T), and IL-1β, IL-6, TNF-α, IL-10, and IL-4 in the peripheral blood plasma of normal people, patients with depression, and patients with DCMI were measured. Then, the levels of IL-1β, IL-6, TNF-α, IL-10, IL-4, β-catenin in rat testis and peripheral blood and ANXA2, APP, SEMG1, and SEMG2 in seminal plasma proteins were examined. Moreover, the level of β-catenin in the testicular tissue was detected. LPS was used to treat Sertoli cells, and the level of β-catenin was detected. Finally, we evaluated the reproductive phenotype and sperm motility of rats. Results. BA (especially 100 mg/kg) could notably ameliorate depression-like behavior induced by CUMS + LPS. The levels of IL-4, IL-10, T, and NPY in depression patients, DCMI patients, and CUMS + LPS model rats elevated, while the levels of IL-1β, IL-6, and TNF-α were reduced. However, BA alleviated the changes in these factors. Moreover, BA alleviated male rat depression induced by CUMS + LPS. LPS upregulated β-catenin (NP) but could not adjust β-catenin (TP) level in rat Sertoli cells. BA relieved the symptoms of DCMI by regulating β-catenin. Furthermore, BA ameliorated the reproductive ability of depressed rats. Conclusion. BA modulated β-catenin in the relief of inflammatory factor-induced DCMI.