Effects of <i>Cordyceps cicadae</i> Polysaccharide on Gut Microbiota, the Intestinal Mucosal Barrier, and Inflammation in Diabetic Mice
<b>Background:</b> Polysaccharides produced by the edible fungus <i>Cordyceps cicadae</i> can regulate blood sugar levels and may represent a suitable candidate for the treatment of diabetes and its complications. However, there is limited information available about the mech...
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author | Lijia Sun Huaibo Yuan Huiqing Ma Yani Wang |
author_facet | Lijia Sun Huaibo Yuan Huiqing Ma Yani Wang |
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description | <b>Background:</b> Polysaccharides produced by the edible fungus <i>Cordyceps cicadae</i> can regulate blood sugar levels and may represent a suitable candidate for the treatment of diabetes and its complications. However, there is limited information available about the mechanism of how <i>C. cicadae</i> polysaccharide (CCP) might improve diabetic conditions. <b>Methods:</b> This study investigated its effects on the intestinal microbiota, intestinal mucosal barrier, and inflammation in mice with type 2 diabetes mellitus (T2DM) induced by streptozotocin, and its potential mechanisms. <b>Results:</b> Compared with the DC (diabetes model control group), CCPH oral treatment significantly increased the number of beneficial bifidobacteria, bifidobacteria, and lactobacilli (<i>p</i> < 0.01), restored the diversity of intestinal microorganisms in diabetic mice, and the proportions of Firmicutes and Bacteroidetes (34.36%/54.65%) were significantly lower than those of the DC (52.15%/32.09%). Moreover, CCPH significantly reduced the content of endotoxin (lipopolysaccharide, LPS) and D-lactic acid(D-LA) (<i>p</i> < 0.05), the activities of antioxidant enzymes and total antioxidant capacity were significantly increased (<i>p</i> < 0.01), and the content of proinflammatory cytokines TNF-α, IL-6, and IL-1β were reduced by 42.05%, 51.28%, and 52.79%, respectively, compared with the DC. The TLR4/NF-κB signaling pathway, as a therapeutic target for diabetic intestinal diseases, plays a role in regulating the inflammatory response and protecting the intestinal barrier function. Molecular mechanism studies showed that oral treatment with CCPH down-regulated the expression of NF-κB, TLR-4, and TNF-α genes by 18.66%, 21.58%, and 34.87%, respectively, while up-regulating the expression of ZO-1 and occludin genes by 32.70% and 25.11%, respectively. CCPH regulates the expression of short-chain fatty acid levels, increases microbial diversity, and ameliorates mouse colon lesions by inhibiting the TLR4/NF-κB signaling pathway. <b>Conclusions:</b> In conclusion, it is demonstrated that in this murine model, the treatment of diabetes with <i>C. cicadae</i> polysaccharide can effectively regulate intestinal microbiota imbalance, protect intestinal mucosal barrier function, and reduce inflammation in vivo, suggesting this natural product can provide a suitable strategy for the treatment of T2D-induced gut dysbiosis and intestinal health. |
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spelling | doaj-art-3855b775bc794ac0910f3c7e4eb429f72025-01-24T13:41:08ZengMDPI AGMetabolites2218-19892025-01-01151810.3390/metabo15010008Effects of <i>Cordyceps cicadae</i> Polysaccharide on Gut Microbiota, the Intestinal Mucosal Barrier, and Inflammation in Diabetic MiceLijia Sun0Huaibo Yuan1Huiqing Ma2Yani Wang3School of Food and Biological Engineering, Hefei University of Technology, No. 193, Tunxi Road, Hefei 230009, ChinaSchool of Food and Biological Engineering, Hefei University of Technology, No. 193, Tunxi Road, Hefei 230009, ChinaSchool of Food and Biological Engineering, Hefei University of Technology, No. 193, Tunxi Road, Hefei 230009, ChinaSchool of Food and Biological Engineering, Hefei University of Technology, No. 193, Tunxi Road, Hefei 230009, China<b>Background:</b> Polysaccharides produced by the edible fungus <i>Cordyceps cicadae</i> can regulate blood sugar levels and may represent a suitable candidate for the treatment of diabetes and its complications. However, there is limited information available about the mechanism of how <i>C. cicadae</i> polysaccharide (CCP) might improve diabetic conditions. <b>Methods:</b> This study investigated its effects on the intestinal microbiota, intestinal mucosal barrier, and inflammation in mice with type 2 diabetes mellitus (T2DM) induced by streptozotocin, and its potential mechanisms. <b>Results:</b> Compared with the DC (diabetes model control group), CCPH oral treatment significantly increased the number of beneficial bifidobacteria, bifidobacteria, and lactobacilli (<i>p</i> < 0.01), restored the diversity of intestinal microorganisms in diabetic mice, and the proportions of Firmicutes and Bacteroidetes (34.36%/54.65%) were significantly lower than those of the DC (52.15%/32.09%). Moreover, CCPH significantly reduced the content of endotoxin (lipopolysaccharide, LPS) and D-lactic acid(D-LA) (<i>p</i> < 0.05), the activities of antioxidant enzymes and total antioxidant capacity were significantly increased (<i>p</i> < 0.01), and the content of proinflammatory cytokines TNF-α, IL-6, and IL-1β were reduced by 42.05%, 51.28%, and 52.79%, respectively, compared with the DC. The TLR4/NF-κB signaling pathway, as a therapeutic target for diabetic intestinal diseases, plays a role in regulating the inflammatory response and protecting the intestinal barrier function. Molecular mechanism studies showed that oral treatment with CCPH down-regulated the expression of NF-κB, TLR-4, and TNF-α genes by 18.66%, 21.58%, and 34.87%, respectively, while up-regulating the expression of ZO-1 and occludin genes by 32.70% and 25.11%, respectively. CCPH regulates the expression of short-chain fatty acid levels, increases microbial diversity, and ameliorates mouse colon lesions by inhibiting the TLR4/NF-κB signaling pathway. <b>Conclusions:</b> In conclusion, it is demonstrated that in this murine model, the treatment of diabetes with <i>C. cicadae</i> polysaccharide can effectively regulate intestinal microbiota imbalance, protect intestinal mucosal barrier function, and reduce inflammation in vivo, suggesting this natural product can provide a suitable strategy for the treatment of T2D-induced gut dysbiosis and intestinal health.https://www.mdpi.com/2218-1989/15/1/8<i>Cordyceps cicadae</i> polysaccharidesdiabetes mellitusintestinal floraintestinal mucosal barrierinflammation |
spellingShingle | Lijia Sun Huaibo Yuan Huiqing Ma Yani Wang Effects of <i>Cordyceps cicadae</i> Polysaccharide on Gut Microbiota, the Intestinal Mucosal Barrier, and Inflammation in Diabetic Mice Metabolites <i>Cordyceps cicadae</i> polysaccharides diabetes mellitus intestinal flora intestinal mucosal barrier inflammation |
title | Effects of <i>Cordyceps cicadae</i> Polysaccharide on Gut Microbiota, the Intestinal Mucosal Barrier, and Inflammation in Diabetic Mice |
title_full | Effects of <i>Cordyceps cicadae</i> Polysaccharide on Gut Microbiota, the Intestinal Mucosal Barrier, and Inflammation in Diabetic Mice |
title_fullStr | Effects of <i>Cordyceps cicadae</i> Polysaccharide on Gut Microbiota, the Intestinal Mucosal Barrier, and Inflammation in Diabetic Mice |
title_full_unstemmed | Effects of <i>Cordyceps cicadae</i> Polysaccharide on Gut Microbiota, the Intestinal Mucosal Barrier, and Inflammation in Diabetic Mice |
title_short | Effects of <i>Cordyceps cicadae</i> Polysaccharide on Gut Microbiota, the Intestinal Mucosal Barrier, and Inflammation in Diabetic Mice |
title_sort | effects of i cordyceps cicadae i polysaccharide on gut microbiota the intestinal mucosal barrier and inflammation in diabetic mice |
topic | <i>Cordyceps cicadae</i> polysaccharides diabetes mellitus intestinal flora intestinal mucosal barrier inflammation |
url | https://www.mdpi.com/2218-1989/15/1/8 |
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