To investigate the structure-activity relationship of polysaccharide and obtain a better antidepressant polysaccharide, the antidepressant-like activity of a carboxymethyl polysaccharide (C-MEPS2) subjected to submerged fermentation was systematically studied. PC12-H cell and Kunming mice were used to investigate the differences and their mechanism in the antidepressant effects of C-MEPS2 and MEPS2. Cell experiments have showed that C-MEPS2 has a better antidepressant effect than MEPS2. C-MEPS2 could exert antidepressant effects related to catecholamine synthesis with specific sites of TH, D2DR, and P-CAMKII. In addition, C-MEPS2 could repair the Res-induced damage in PC12-H cell, stabilize the mitochondrial membrane potential and regulate intracellular Ca²⁺ concentration, thus reducing cell apoptosis caused by RES. Antagonists common dosing experiments on animals further proved that CMEPS2 could significantly improve the antidepressant effect of derivatives without affecting the antidepressant mechanism of MEPS2. It is speculated that it may be related to carboxymethylated modification.

Monascus vinegar (MV) is a typical fermented food with various health-promoting effects. This study aimed to evaluate the role of MV in alleviating high-fat-diet-induced inflammation in rats with hyperlipidemia and elucidate the possible regulatory mechanisms. In the study, serum lipid profiles, liver pathology and liver inflammatory cytokines were analyzed in hyperlipidemia rats with MV (0.5 mL/kg m_b, 2 mL/kg m_b). Results showed that the administration of MV alleviated dyslipidemia by decreasing the serum and liver levels of triglyceride and total cholesterol. Increase in hepatic lipase and carnitine palmitoyl transferase 1 (CPT-1) levels and decrease in hepatocyte steatosis, nephritis, and intestinal tissue injury in the HD group showed that high-dose MV can significantly suppress hepatic lipid accumulation and steatosis. In addition, compared with the model (MOD) group, the HD group showed significantly down-regulated the level of serum or hepatic alanine aminotransferase (ALT), aspartate aminotransferase (AST), CPT-1, interleukin (IL)-2, IL-6, IL-12, and tumor necrosis factor α (TNF-α). Moreover, the HD group showed repressed hepatic nuclear factor κB (NF-κB) pathway and inactivated phosphatidylinositol 3-kinase (PI3K)/ protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway mitigated liver inflammation. Similar results were obtained from cell experiments. Collectively, these findings revealed that MV might attenuate high-fat-diet-induced inflammation by inhibiting the NF-κB and PI3K/Akt/mTOR pathways.