Polysaccharides are closely associated with immune regulation, but there are different polysaccharide effects from different sources. In this study, the aim was to investigate the effect of tremella polysaccharides (TP) in cyclophosphamide-induced immunodeficient mice. We observed the thymus and spleen index, liver and spleen pathological changes, and the levels of IL-2, IL-12, INF-γ, TGF-β and Ig G in serum, and we also noted the mRNA expression of IL-1β, IL-4, IL-12 and TGF-β in liver and spleen. Besides, we also measured the best effects of different doses of TP (Low-TP was 20 mg/kg·BW, Middle-TP was 40 mg/kg·BW, and High-TP was 80 mg/kg·BW) on cyclophosphamide-induced immunosuppressed mice. The results were remarkable, and suggested that TP had a significant effect for enhancing immunity in cyclophosphamide-induced immunosuppression, and the immune enhancement of High-TP had the best results in TP-treated mice. It could significantly increase the thymus and spleen index, alleviate pathological features of immunosuppression such as the arrangement of liver sinusoid and hepatic plates was disordered, massive inflammatory cells infiltrated and fatty degeneration of hepatocytes in liver, and red pulp and white pulp were intermixed, splenic corpuscles demolished and disappeared, splenic sinusoid extended, and lymphocytes of spleen were reduced in spleen. Besides, it could also up-regulate serum levels of IL-2, IL-12, INF-γ and Ig G, reduce the level of TGF-β in serum, markedly promote mRNA expression of IL-1β, IL-4 and IL-12 in liver and spleen, and suppress mRNA expression of TGF-β. Above all, TP showed preventive effect for cyclophosphamide-induced immunosuppressed mice.

The purpose of the study was to determine the inhibitory effects of Lactobacillus fermentum Suo (LF-Suo) on HCl/ethanol induced gastric injury in ICR (Institute for Cancer Research) mice and explain the mechanism of these effects through the molecular biology activities of LF-Suo. The studied mice were divided into four groups: healthy, injured, LF-Suo-L and LF-Suo-H group. After the LF-Suo intragastric administration, the gastric injury area was reduced compared to the injured group. The serum MOT (motilin), SP (substance P), ET (endothelin) levels of LF-Suo treated mice were lower, and SS (somatostatin), VIP (vasoactive intestinal peptide) levels were higher than the injured group mice. The cytokine IL-6 (interleukin 6), IL-12 (interleukin 12), TNF-α (tumor necrosis factor-α) and IFN-γ (interferon-γ) serum levels were decreased after the LF-Suo treatment. The gastric tissues SOD (superoxide dismutase), GSH-Px (glutathione peroxidase), NO (nitric oxide) and activities of LF-Suo treated mice were increased and MDA (malondialdehyde) activity was decreased compared to the injured group mice. By the RT-PCR assay, LF-Suo raised the occludin, EGF (epidermal growth factor), EGFR (epidermal growth factor receptor), VEGF (vascular endothelial growth factor), Fit-1 (fms-like tyrosine kinase-1), IκB-α (inhibitor kappaB-α), nNOS (neuronal nitric oxide synthase), eNOS (endothelial nitric oxide synthase), Mn-SOD, Cu/Zn-SOD, CAT (catalase) mRNA or protein expressions and reduced the COX-2, NF-κB (nuclear factor kappaB), and iNOS (inducible nitric oxide synthase) expressions in gastric tissues compared to the gastric injured group mice. A high concentration (1.0 × 10⁹ CFU/kg b.w.) of LF-Suo treatment showed stronger anti-gastric injury effects compared to a low concentration of (0.5 × 10⁹ CFU/kg b.w.) of LF-Suo treatment. LF-Suo also showed strong survival in pH 3.0 man-made gastric juice and hydrophobic properties. These results indicate that LF-Suo has potential use as probiotics for its gastric injury treatment effects.

The aim of this study is to assess the preventive effects of Lactobacillus fermentum HY01 (LF-HY01) to dextran sulfate sodium induced-colitis. We observed the ratio of colon weight to its length, colon pathological changes, and the concentrations of pro-inflammatory factors (IFN-γ, IL-12, TNFα, and IL-6) in serum. We also took account of the protein levels of IκBα, NF-κB p65, iNOS, and COX-2, and we measured the best effects of different doses of Lactobacillus fermentum HY01 (low dose group was 10⁹ CFU/kg·bw, high dose group was 10¹⁰ CFU/kg·bw) on dextran sulfate sodium-induced colitis mice. The results were remarkable, suggesting that Lactobacillus fermentum HY01 had significant preventive effects in dextran sulfate sodium induced-colitis; simultaneously, the high dose group showed the best results among other groups. It can effectively alleviate the shortened colon length, reduce the ratio of colon weight to its length, reduce edema, inflammatory cells infiltration, and colon mucosa injury, and play an important role in the down-regulation of concentrations of pro-inflammatory factors (IFN-γ, IL-12, TNFα, and IL-6). Above all, Lactobacillus fermentum HY01 shows promising prevention for IκBα degradation, inhibition of NF-κB p65 phosphorylation cascades, and decreases the protein levels of iNOS and COX-2 as well.

A high-fat diet-induced C57BL/6N mouse model of non-alcoholic fatty liver disease (NAFLD) was established. The effect and mechanism of Raw Bowl Tea polyphenols (RBTP) on preventing NAFLD via regulating intestinal function were observed. The serum, liver, epididymis, small intestine tissues, and feces of mice were examined by biochemical and molecular biological methods, and the composition of RBTP was analyzed by HPLC assay. The results showed that RBTP could effectively reduce the body weight, liver weight, and liver index of NAFLD mice. The serum effects of RBTP were: (1) decreases in alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (AKP), total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), D-lactate (D-LA), diamine oxidase (DAO), lipopolysaccharide (LPS), and an increase of high density lipoprotein cholesterol (HDL-C) levels; (2) a decrease of inflammatory cytokines such as interleukin 1 beta (IL-1β), interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor alpha (TNF-α), and interferon gamma (INF-γ); (3) a decrease the reactive oxygen species (ROS) level in liver tissue; and (4) alleviation of pathological injuries of liver, epididymis, and small intestinal tissues caused by NAFLD and protection of body tissues. qPCR and Western blot results showed that RBTP could up-regulate the mRNA and protein expressions of LPL, PPAR-α, CYP7A1, and CPT1, and down-regulate PPAR-γ and C/EBP-α in the liver of NAFLD mice. In addition, RBTP up-regulated the expression of occludin and ZO-1, and down-regulated the expression of CD36 and TNF-α in the small intestines of NAFLD mice. Studies on mice feces showed that RBTP reduced the level of Firmicutes and increased the minimum levels of Bacteroides and Akkermansia, as well as reduced the proportion of Firmicutes/Bacteroides in the feces of NAFLD mice, which play a role in regulating intestinal microecology. Component analysis showed that RBTP contained seven polyphenolic compounds: Gallic acid, (-)-epigallocatechin, catechin, L-epicatechin, (-)-epigallocatechin gallate, (-)-gallocatechin gallate, and (-)-epicatechin gallate (ECG), and high levels of caffeine, (-)-epigallocatechin (EGC), and ECG. RBTP improved the intestinal environment of NAFLD mice with the contained active ingredients, thus playing a role in preventing NAFLD. The effect was positively correlated with the dose of 100 mg/kg, which was even better than that of the clinical drug bezafibrate.

The present study investigated the preventive effect of polyphenols in Liubao tea (PLT) on carbon tetrachloride (CCl₄)-induced liver injury in mice. The mice were initially treated with PLT, followed by induction of liver injury using 10 mL/kg CCl₄. Then liver and serum indices, as well as the expression levels of related messenger RNAs (mRNAs) and proteins in liver tissues were measured. The results showed that PLT reduces the liver quality and indices of mice with liver injury. PLT also downregulates aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglycerides (TGs), and malondialdehyde (MDA), and upregulates superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the sera of mice with liver injury. PLT also reduces serum levels of interleukin-6 (IL-6), interleukin-12 (IL-12), tumor necrosis factor- $\mathsf{\alpha }$ (TNF- $\mathsf{\alpha }$ ), and interferon- $\mathsf{\gamma }$ (IFN- $\mathsf{\gamma }$ ) cytokines in mice with liver injury. Pathological morphological observation also shows that PLT reduces CCl₄-induced central venous differentiation of liver tissues and liver cell damage. Furthermore, qPCR and Western blot also confirm that PLT upregulates the mRNA and protein expressions of Gu/Zn-SOD, Mn-SOD, catalase (CAT), GSH-Px, and nuclear factor of $\mathsf{\kappa }$ -light polypeptide gene enhancer in B-cells inhibitor- $\mathsf{\alpha }$ (I $\mathsf{\kappa }$ B- $\mathsf{\alpha }$ ) in liver tissues, and downregulates the expression of cyclooxygenase 2 (COX-2) and nuclear factor $\mathsf{\kappa }$ -light-chain-enhancer of activated B cells (NF- $\mathsf{\kappa }$ B). Meanwhile, PLT also raised the phosphorylated (p)-NF- $\mathsf{\kappa }$ B p65 and cytochrome P450 reductase protein expression in liver injury mice. The components of PLT include gallic acid, catechin, caffeine, epicatechin (EC), epigallocatechin gallate (EGCG), gallocatechin gallate (GCG), and epicatechin gallate (ECG), which possibly have a wide range of biological activities. Thus, PLT imparts preventive effects against CCl₄-induced liver injury, which is similar to silymarin.

The aim of this study was to investigate and compare the effects of heat-killed and live Lactobacillus on carbon tetrachloride (CCl₄)-induced acute liver injury mice. The indexes evaluated included liver pathological changes, the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the serum, related gene expression (IL-1β, TNF-α, Bcl-2, and Bax), and related proteins levels (Bax, Bcl-2, Caspase 3, and NF-κB p65). Compared with the model group, the results indicated that the levels of ALT, AST, and MDA in the serum, the expression levels of IL-1β, TNF-α, and Bax, and the protein levels of Bax, Caspase 3, and NF-κB p65 significantly decreased, and the pathologic damage degree all significantly reduced after live Lactobacillus fermentum (L-LF) and live Lactobacillus plantarum (L-LP) treatment. Additionally, the levels of SOD and GSH in the serum, the gene expression of Bcl-2, and the protein level of Bcl-2 significantly increased after L-LF and L-LP treatment. Although HK-LF and HK-LP could also have obvious regulating effects on some of the evaluated indexes (ALT, AST, the expression levels of TNF-α and Bax, and the protein level of Bcl-2) and play an important role in weakening liver damage, the regulating effects of L-LF or L-LP on these indexes were all better compared with the corresponding heat-killed Lactobacillus fermentum (HK-LF) and heat-killed Lactobacillus plantarum (HK-LP). Therefore, these results suggested that LF and LP have an important role in liver disease.