<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ji J</submitter><funding>Fundamental Research Funds for the Central Universities</funding><funding>Start-Up Funds of Introduced Talent in Lanzhou University</funding><funding>National Natural Science Foundation of China</funding><funding>Natural Science Foundation of Gansu Province</funding><pagination>183</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12375036</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9(1)</volume><pubmed_abstract>Reducing intestinal absorption by degrading purine nucleosides has been shown to alleviate hyperuricemia (HUA). The probiotic Pediococcus acidilactici GR-5, derived from the traditional food "Jiangshui", achieved efficient degradation of purine nucleosides through its unique purine nucleoside phosphorylase-DeoD. In the purine nucleosides-induced HUA mouse model, GR-5 treatment reduced serum uric acid (UA) by about 52.17%. GR-5 may improves tissue inflammatory damage by inhibiting the NLRP3 inflammatory pathway, and restored the intestinal barrier by increasing tight junction proteins Occludin and ZO-1 expression, which outperforming the allopurinol. The mechanism of UA reduction may also involves inhibiting UA synthase activity and regulating UA transporters level. GR-5 colonization in intestine increased the abundance of Lactobacillus, improved the metabolism of purine, tryptophan and bile acid by gut microbiota, and increased the level of SCFAs. Overall, GR-5 may be a potential preventive agent for improving HUA and is expected to provide a healthy option for preventing diet-induced HUA.</pubmed_abstract><journal>NPJ science of food</journal><pubmed_title>Pediococcus acidilactici GR-5 alleviates hyperuricemia by degrading purine nucleosides and improving gut microbiota metabolism.</pubmed_title><pmcid>PMC12375036</pmcid><funding_grant_id>561120220</funding_grant_id><funding_grant_id>24ZDWA005</funding_grant_id><funding_grant_id>24JRRA519</funding_grant_id><funding_grant_id>32300049</funding_grant_id><funding_grant_id>lzujbky-2023-pd11</funding_grant_id><funding_grant_id>32370110</funding_grant_id><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Salama ES</pubmed_authors><pubmed_authors>An ZY</pubmed_authors><pubmed_authors>Yun H</pubmed_authors><pubmed_authors>Jin WL</pubmed_authors><pubmed_authors>Liu P</pubmed_authors><pubmed_authors>Khan A</pubmed_authors><pubmed_authors>Kulshreshtha S</pubmed_authors><pubmed_authors>Ji J</pubmed_authors><pubmed_authors>Peng L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pediococcus acidilactici GR-5 alleviates hyperuricemia by degrading purine nucleosides and improving gut microbiota metabolism.</name><description>Reducing intestinal absorption by degrading purine nucleosides has been shown to alleviate hyperuricemia (HUA). The probiotic Pediococcus acidilactici GR-5, derived from the traditional food "Jiangshui", achieved efficient degradation of purine nucleosides through its unique purine nucleoside phosphorylase-DeoD. In the purine nucleosides-induced HUA mouse model, GR-5 treatment reduced serum uric acid (UA) by about 52.17%. GR-5 may improves tissue inflammatory damage by inhibiting the NLRP3 inflammatory pathway, and restored the intestinal barrier by increasing tight junction proteins Occludin and ZO-1 expression, which outperforming the allopurinol. The mechanism of UA reduction may also involves inhibiting UA synthase activity and regulating UA transporters level. GR-5 colonization in intestine increased the abundance of Lactobacillus, improved the metabolism of purine, tryptophan and bile acid by gut microbiota, and increased the level of SCFAs. Overall, GR-5 may be a potential preventive agent for improving HUA and is expected to provide a healthy option for preventing diet-induced HUA.</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Aug</publication><modification>2026-05-09T17:48:54.183Z</modification><creation>2026-04-08T01:08:16.572Z</creation></dates><accession>S-EPMC12375036</accession><cross_references><pubmed>40849527</pubmed><doi>10.1038/s41538-025-00556-y</doi></cross_references></HashMap>