Polysaccharide decolorization is a key determinant of polysaccharide structure. In this study, two purified Rehmannia glutinosa polysaccharides, RGP−1−A and RGP−2−A, were obtained after decolorization using the AB-8 macroporous resin and H₂O₂, respectively. RGP−1−A (molecular weight (Mw) = 18,964 Da) and RGP−2−A (Mw = 3305 Da) were acidic and neutral heteropolysaccharides, respectively, and were both polycrystalline in structure. FTIR analysis revealed that RGP−1−A was a sulfate polysaccharide, while RGP−2−A had no sulfate group. Experiments on IPEC-1 cells showed that RGPs alleviated oxidative stress by regulating the Nrf2/Keap1 pathway. These findings were confirmed by the upregulation of Nrf2, NQO1, and HO-1; the subsequent increase in the levels of antioxidant indicators (SOD, LDH, CAT, and MDA); and the restoration of mitochondrial membrane potential. Overall, the antioxidant capacity of RGP−1−A was significantly higher than that of RGP−2−A. These results suggest that RGPs may be a potential natural antioxidant and could be developed into functional foods.

Polysaccharide decolorization has a major effect on polysaccharide function. In the present study, the decolorization of Rehmannia glutinosa polysaccharides (RGP) is optimized using two methods—the AB-8 macroporous resin (RGP-1) method and the H₂O₂ (RGP-2) method. The optimal decolorization parameters for the AB-8 macroporous resin method were as follows: temperature, 50 °C; macroporous resin addition, 8.4%; decolorization duration, 64 min; and pH, 5. Under these conditions, the overall score was 65.29 ± 3.4%. The optimal decolorization conditions for the H₂O₂ method were as follows: temperature, 51 °C; H₂O₂ addition, 9.5%; decolorization duration, 2 h; and pH, 8.6. Under these conditions, the overall score was 79.29 ± 4.8%. Two pure polysaccharides (RGP-1-A and RGP-2-A) were isolated from RGP-1 and RGP-2. Subsequently, their antioxidant and anti-inflammatory effects and mechanisms were evaluated. RGP treatment activated the Nrf2/Keap1 pathway and significantly increased the activity of antioxidant enzymes (p < 0.05). It also inhibited the expression of pro-inflammatory factors and suppressed the TLR4/NF-κB pathway (p < 0.05). RGP-1-A had a significantly better protective effect than RGP-2-A, likely owing to the sulfate and uronic groups it contains. Together, the findings indicate that RGP can act as a natural agent for the prevention of oxidation and inflammation-related diseases.

Enterotoxigenic Escherichia coli (ETEC) infection is one of the most common bacterial causes of diarrhea in children and young farm animals. Medium-chain fatty acids (MCFAs) have been widely used for their antibacterial and immune functions. However, there is limited information regarding the role of MCFAs chelated with Zn in diarrhea induced by ETEC infection. Here, zinc laurate (ZnLa) was used to evaluate its protective effect in a mice diarrhea model induced by ETEC. A total of 45 ICR-weaned female mice were randomly assigned to marginal zinc deficiency (dZn), dZn, and ETEC infection groups (dZn+ETEC); ETEC infection was co-treated with a low, middle, or high dose of ZnLa (ZnLa LOW+ETEC, ZnLa MID+ETEC, and ZnLa HIGH+ETEC), respectively, to explore the effect and its mechanism of ZnLa on diarrhea and intestinal health of mice challenged with ETEC. To further compare the antibacterial efficiency of ZnLa and ZnSO₄ in mice with ETEC infection, a total of 36 ICR-weaned female mice were randomly divided into ZnLa, ZnLa+ETEC, ZnSO₄, and ZnSO₄ and ETEC infection groups (ZnSO₄+ETEC); moreover, the growth curve of ETEC also compared ZnLa and ZnSO₄ in vitro. Mice pretreated with ZnLa were effectively guarded against body weight losses and increases in diarrhea scores induced by ETEC. ZnLa pretreatment also prevented intestinal barrier damage and ion transport in mice challenged with ETEC, as evidenced by the fact that the intestinal villus height and the ratio of villus height and crypt depth, tight junction protein, and Na⁺ absorption were higher, whereas intestinal permeability and anion secretion were lower in mice pretreated with ZnLa. In addition, ZnLa conferred effective protection against ETEC-induced intestinal inflammatory responses, as the increases in protein and mRNAs of proinflammatory cytokines were prevented in serum and jejunum, which was likely associated with the TLR4/MYD88/NF-κB signaling pathway. The increase in ETEC shedding and virulence-related gene expression was prevented in mice with ZnLa pretreatment. Finally, the growth of ETEC and virulence-related gene expression were lower in the ZnLa group than in ZnSO₄ with an equal concentration of zinc. These findings suggest that ZnLa is a promising prevention strategy to remedy ETEC infection.

Abnormally elevated circulating bile acids (BA) during pregnancy endanger fetal survival and offspring health; however, the pathology and underlying mechanisms are poorly understood. A total of nineteen pregnant sows were randomly assigned to day 60 of gestation, day 90 of gestation (G60, G90), and the farrowing day (L0), to investigate the intercorrelation of reproductive hormone, including estradiol, progesterone and sulfated progesterone metabolites (PMSs), and BA in the peripheral blood of mother and fetuses during pregnancy. All data were analyzed by Student’s t-test or one-way ANOVA of GraphPad Prism and further compared by using the Student–Newman–Keuls test. Correlation analysis was also carried out using the CORR procedure of SAS to study the relationship between PMSs and BA levels in both maternal and fetal serum at G60, G90, and L0. Allopregnanolone sulphate (PM4S) and epiallopregnanolone sulphate (PM5S) were firstly identified in the maternal and fetal peripheral blood of pregnant sows by using newly developed ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) methods. Correlation analysis showed that pregnancy-associated maternal BA homeostasis was correlated with maternal serum PM4S levels, whereas fetal BA homeostasis was correlated with fetal serum PM5S levels. The antagonist activity role of PM5S on farnesoid X receptor (FXR)-mediated BA homeostasis and fibroblast growth factor 19 (FGF19) were confirmed in the PM5S and FXR activator co-treated pig primary hepatocytes model, and the antagonist role of PM4S on FXR-mediated BA homeostasis and FGF19 were also identified in the PM4S-treated pig primary hepatocytes model. Together with the high relative expression of FGF19 in pig hepatocytes, the pregnant sow is a promising animal model to investigate the pathogenesis of cholestasis during pregnancy.

Zinc is both essential and inhibitory for the pathogenesis of enterotoxigenic Escherichia coli (ETEC). However, the accurate effects and underlying mechanism of marginal zinc deficiency on ETEC infection are not fully understood. Here, a marginal zinc-deficient mouse model was established by feeding mice with a marginal zinc-deficient diet, and ETEC k88 was further administrated to mice after antibiotic disruption of the normal microbiota. Marginal zinc deficiency aggravated growth impairment, diarrhea, intestinal morphology, intestinal permeability, and inflammation induced by ETEC k88 infection. In line with the above observations, marginal zinc deficiency also increased the intestinal ETEC shedding, though the concentration of ETEC in the intestinal content was not different or even decreased in the stool. Moreover, marginal zinc deficiency failed to change the host’s zinc levels, as evidenced by the fact that the serum zinc levels and zinc-receptor GPR39 expression in jejunum were not significantly different in mice with ETEC challenge. Finally, marginal zinc deficiency upregulated the relative expression of virulence genes involved in heat-labile and heat-stable enterotoxins, motility, cellular adhesion, and biofilm formation in the cecum content of mice with ETEC infection. These findings demonstrated that marginal zinc deficiency likely regulates ETEC infection through the virulence factors, whereas it is not correlated with host zinc levels.

Lactobacillus rhamnosus GG alleviates LPS-induced liver injury by restoring TDCA through enhanced bile acid reabsorption and gut microbiota modulation. TDCA mitigates inflammation partially through the oxidative phosphorylation pathway.