Lactic acid bacteria strain (LAB) NCU116 fermented Asparagus officinalis polysaccharides (FAOP) have been proven to cause substantial changes in physicochemical properties such as monosaccharide composition and molecular weight, accounting for their enhanced immune activity than unprocessed Asparagus officinalis polysaccharides (AOP). In the current study, the hepatoprotective effects of FAOP in mice with cyclophosphamide (CTX)-induced hepatotoxicity were investigated. FAOP were more effective than AOP in alleviating CTX-induced hepatic damage, including inhibition of hepatic biochemical markers (ALT, AST, AKP and LDH) and pro-inflammatory cytokines (TNF-α and IL-1β) as well as reinforcement of antioxidant systems (T-AOC, SOD, CAT, and MDA). In particular, compared with AOP, FAOP showed superior performance by promoting GSH biosynthesis, and normalizing the expression level of bile acid receptors (FXR and SHP) and key enzymes in bile acid synthesis (CYP7A1, CYP8B1 and CYP27A1). Modulation of disordered homeostasis of bile acids by FAOP can be attributed to the upregulation of hepatic short chain fatty acid (SCFA) receptors GPR41 and GPR109A as well as intestinal SCFA production. Furthermore, serum metabolomics study validated the hepatoprotective superiority of FAOP than AOP with evidence from variations in bile acid compositions and the construction of related metabolic pathways. Therefore, LAB NCU116 fermentation of Asparagus officinalis was practical and effective to obtain promising hepatoprotective polysaccharides, which might arise from enhanced SCFA production than unprocessed AOP.

Background: Nanoplastics (NPs) are omnipresent in our lives as a new type of pollution with a tiny size. It can enter organisms from the environment, accumulate in the body, and be passed down the food chain. Inflammatory bowel disease (IBD) is a nonspecific intestinal inflammatory disease that is recurrent and prevalent in the population. Given that the intestinal features of colitis may affect the behavior and toxicity of NPs, it is imperative to clarify the risk and toxicity mechanisms of NPs in colitis models. Methods and results: In this study, mice were subjected to three cycles of 5-day dextran sulfate sodium (DSS) exposures, with a break of 7 to 11 days between each cycle. After the first cycle of DSS exposure, the mice were fed gavagely with water containing 100 nm polystyrene nanobeads (PS-NPs, at concentrations of 1 mg/kg·BW, 5 mg/kg·BW and 25 mg/kg·BW, respectively) for 28 consecutive days. The results demonstrated that cyclic administration of DSS induced chronic inflammation in mice, while the standard drug “5-aminosalicylic acid (5-ASA)” treatment partially improved colitis manifestations. PS-NPs exacerbated intestinal inflammation in mice with chronic colitis by activating the MAPK signaling pathway. Furthermore, PS-NPs aggravated inflammation, oxidative stress, as well as hepatic lipid metabolism disturbance in the liver of mice with chronic colitis. Conclusion: PS-NPs exacerbate intestinal inflammation and injury in mice with chronic colitis. This finding highlights chronically ill populations’ susceptibility to environmental hazards, which urgent more research and risk assessment studies.

Previous studies have proven that polysaccharide obtained from the seeds of Plantago asiatica L. (PLCP) could induce maturation of murine dendritic cells, promote defecation, and possess antioxidant activity in vitro. However, the effect of PLCP on lipopolysaccharide (LPS)-induced liver injury in mice has been rarely reported. In this study, we investigated the anti-inflammatory effect of PLCP on LPS-induced liver injury. Mice were pretreated orally with different dose of PLCP for 3 weeks. On day 22, they were injected intraperitoneally with LPS and sacrificed 12 h later. The results showed that PLCP inhibited the excessive production of tumor necrosis factor-α, interleukin (IL)-6, IL-10, IL-2, and IL-1β in mouse serum and liver. PLCP also improved glutathione peroxidase and total antioxidant capacity activities in mouse liver. In addition, PLCP inhibited nitric oxide, inducible nitric oxide synthase, and cyclooxygenase-2 expression, and increased metallothionein production in mouse liver. Consequently, PLCP may possess protective effects on inflammatory associated liver injury.

The interplay among gut microbiota, intestines, and liver is crucial in preventing acute alcoholic liver injury. In this study, the hepatoprotective potential of polysaccharides from Eucommia ulmoides Oliv. leaves (EULP) on acute alcoholic liver injury in Kunming male mice was investigated. The structural features suggested that the EULP appeared as a heterogeneous mixture of polysaccharides with a molecular weight of 186132 Da. A 14-day pretreatment of EULP ameliorated acute alcoholic-induced hepatic inflam mation (TNF-α, IL-6, and IL-10), oxidative stress (GSH, SOD, and T-AOC), and liver damage (ALT and AST) via enhancing intestinal barrier (Occludin, Claudin 1, and ZO-1) and modulating microbiome, which subsequently inhibiting endotoxemia and balancing the homeostasis of the gut–liver axis. EULP restored the composition of intestinal flora with an increase in the relative abundance of Lactobacillaceae and a decrease in Lachnospiraceae and Verrucomicrobiaceae. Notably, prolonged EULP pretreatment (14 days) but no single gavage of EULP achieved excellent hepatoprotection. These findings endorsed the potential of EULP as a functional food for mitigating acute alcoholic-induce d liver damage, attributed to its anti-inflammatory, antioxidant, and prebiotic properties facilitated by the microbiota–gut–liver axis.