Yeast Fermentate Prebiotic Ameliorates Allergic Asthma, Associating with Inhibiting Inflammation and Reducing Oxidative Stress Level through Suppressing Autophagy
Autor: | Jing Su, Xiao-Ying Ji, Yina Wang, Bin Xiao, Xudong Xiang, Shaokun Liu, Guyi Wang, Haiyun Dong, Xianghong Yan, Su-bo Gong |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Male Article Subject Immunology ATG5 Inflammation Lung injury medicine.disease_cause DNA Ribosomal Allergic inflammation 03 medical and health sciences Mice 0302 clinical medicine Yeasts medicine Autophagy Pathology Animals RB1-214 Anti-Asthmatic Agents Lung Mice Inbred BALB C medicine.diagnostic_test biology business.industry Cell Biology Sequence Analysis DNA Asthma respiratory tract diseases Ovalbumin Oxidative Stress 030104 developmental biology Bronchoalveolar lavage Prebiotics 030220 oncology & carcinogenesis Fermentation biology.protein medicine.symptom business Bronchoalveolar Lavage Fluid Oxidative stress Biomarkers Research Article Signal Transduction |
Zdroj: | Mediators of Inflammation, Vol 2021 (2021) Mediators of Inflammation |
ISSN: | 1466-1861 0962-9351 |
Popis: | Background and Purpose. Allergic asthma, a respiratory disease with high morbidity and mortality, is reported to be related to the airway allergic inflammation and autophagy-induced oxidative stress. Although the therapeutic effects of fermentate prebiotic (YFP) on allergic asthma have been widely claimed, the underlying mechanism is still unclear. This study is aimed at investigating the possible mechanism for the antiasthma property of YFP in a mouse model. Methods. Ovalbumin was used to induce allergic asthma following administration of YFP for one week in mice, to collect the lung tissues, bronchoalveolar lavage fluid (BLFA), and feces. The pathological state, tight-junction proteins, inflammatory and oxidative stress-associated biomarkers, and TLRs/NF-κB signaling pathway of the lung tissues were evaluated by HE staining, immunofluorescence, ELISA, and WB, separately. RT-PCR was used to test oxidative stress-associated genes. Leukocyte counts of BLFA and intestinal microbiota were also analyzed using a hemocytometer and 16S rDNA-sequencing, separately. Result. YFP ameliorated the lung injury of the mouse asthma model by inhibiting peribronchial and perivascular infiltrations of eosinophils and increasing tight-junction protein expression. YFP inhibited the decrease in the number of BALF leukocytes and expression of inflammatory-related genes and reversed OVA-induced TLRs/NF-κB signaling pathway activation. YFP ameliorated the level of oxidative stress in the lung of the mouse asthma model by inhibiting MDA and promoting the protein level of GSH-PX, SOD, CAT, and oxidative-related genes. ATG5, Beclin1, and LC3BII/I were significantly upregulated in asthma mice, which were greatly suppressed by the introduction of YFP, indicating that YFP ameliorated the autophagy in the lung of the mouse asthma model. Lastly, the distribution of bacterial species was slightly changed by YFP in asthma mice, with a significant difference in the relative abundance of 6 major bacterial species between the asthma and YFP groups. Conclusion. Our research showed that YFP might exert antiasthmatic effects by inhibiting airway allergic inflammation and oxidative stress level through suppressing autophagy. |
Databáze: | OpenAIRE |
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