Weifang Wang,Yunfeng Li,Guojing Han,Aimin Li,Xiaomei Kong
Background Asthma is a chronic disease, which is harmful to the health of the body and the quality of life. Supplementation of Lactobacillus can affect the immune environment of the lungs through the gut-lung axis. This study aimed to explore the potential regulatory targets of Lactobacillus to relieve inflammation in asthma and determine a new approach for improving asthma. Methods A mouse ovalbumin (OVA)-induced model was constructed. OVA mice were supplemented with Lactobacillus fermentum CECT5716 by gavage. The gut microbiota composition of normal and OVA mice was analyzed using 16S ribosomal DNA identification. BALF, serum, lung tissues, and duodenal tissues were collected. Wright’s staining was performed to determine the cell content of the alveolar lavage fluid. Hematoxylin-eosin staining, Masson staining, and periodic acid-Schiff staining were performed to observe the improvement in the lungs of OVA mice supplemented with Lactobacillus . Immunofluorescence was performed to measure the severity of the intestinal barrier leakage. Enzyme-linked immunosorbent assay was carried out to determine the expression levels of inflammatory cell factors, while quantitative reverse transcription-polymerase chain reaction and western blotting were performed to detect the levels of toll-like receptor 2 (TLR2)/TLR4 expression and cell adhesion factors. Results Compared with Control mice, OVA mice exhibited malignant conditions, such as intestinal leakage and lung edema. After supplementation with Lactobacillus , the inflammatory cell content in the bronchoalveolar lavage fluid decreased, and the inflammatory response was alleviated. The level of TLR2/TLR4 expression was reduced. The inflammatory cell infiltration in the airway mucosa of OVA mice was improved, alveolar swelling was reduced and the basement membrane appeared thinner. Conclusion The Lactobacillus inhibited the TLR2/TLR4 expression in OVA mice. Supplementation with Lactobacillus can alleviate the inflammatory response in OVA mice, inhibit pulmonary fibrosis, and treat asthma.
This study aims to evaluate the mechanism of RCH against CCl 4 -induced liver injury in mice. RCH treatment effectively inhibited CCl 4 -induced liver injury and apoptosis in mice, and reduced liver enzyme activities, blood inflammatory cell and serum inflammatory factor levels. Network pharmacology and machine learning predicted that PI3K-Akt pathway and Met proteins play important roles in RCH anti-CCl 4 -induced liver injury. The results of qRT-PCR and Western blot showed that RCH could down-regulate the expression of the receptor proteins Met, Tlr2, and Tlr4, and inhibit the phosphorylation of Pik3ca and Akt1, and prevent the phosphorylation of NF-κB P65, and decrease cleaved Caspase3 expression. These findings suggest that RCH effectively alleviated liver injury in CCl 4 -induced mice by inhibiting the Met/Tlr2/Tlr4-mediated PI3K-Akt signaling pathway.
Liver fibrosis has proven to be the main predisposing factor for liver cirrhosis and liver cancer; however, an effective treatment remains elusive. Polysaccharides , with low toxicity and a wide range of bioactivities, are strong potential candidates for anti-hepatic fibrosis applications. For this study, a new low molecular weight neutral polysaccharide ( B. striata glucomannan (BSP)) was extracted and purified from Bletilla striata . The structure of BSP was characterized and its activities for alleviating liver fibrosis in vivo were further evaluated. The results revealed that the structural unit of BSP was likely →4)-β-D-Glc p -(1 → 4)-β-D-Man p -(1 → 4)-β-D-2ace-Man p -(1 → 4)-β-D-Man p -(1 → 4)-β-D-Glc p -(1 → 4)-β-D-Man p -(1 → 4)-β-D-Man p -(1 → 4)-β-D-3ace-Man p -(1→, with a molecular weight of only 58.5 kDa. Additionally, BSP was observed to attenuate the passive impacts of liver fibrosis in a manner closely related to TLR2/TLR4-MyD88-NF-κB signaling pathway conduction. In summary, the results of this study provide theoretical foundations for the potential applications of BSP as an anti-liver fibrosis platform.
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