<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14(8)</volume><submitter>Li X</submitter><pubmed_abstract>Osteoarthritis (OA) is an aging-associated disease characterized by joint stiffness pain and destroyed articular cartilage. Traditional treatments for OA are limited to alleviating various OA symptoms. There is a lack of drugs available in clinical practice that can truly repair cartilage damage. Here, we developed the chondroitin sulfate analog CS-semi5, semi-synthesized from chondroitin sulfate A. &lt;i>In vivo&lt;/i>, CS-semi5 alleviated inflammation, provided analgesic effects, and protected cartilage in the modified Hulth OA rat model and papain-induced OA rat model. A bioinformatics analysis was performed on samples from OA patients and an exosome analysis on papain-induced OA rats, revealing miR-122-5p as the key regulator associated with CS-semi5 in OA treatment. Binding prediction revea</pubmed_abstract><journal>Acta pharmaceutica Sinica. B</journal><pagination>3528-3542</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11365380</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Semi-synthetic chondroitin sulfate CS-semi5 upregulates miR-122-5p, conferring a therapeutic effect on osteoarthritis &lt;i>via&lt;/i> the p38/MMP13 pathway.</pubmed_title><pmcid>PMC11365380</pmcid><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Wu L</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Yang S</pubmed_authors><pubmed_authors>Zhao Z</pubmed_authors><pubmed_authors>Song Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Semi-synthetic chondroitin sulfate CS-semi5 upregulates miR-122-5p, conferring a therapeutic effect on osteoarthritis &lt;i>via&lt;/i> the p38/MMP13 pathway.</name><description>Osteoarthritis (OA) is an aging-associated disease characterized by joint stiffness pain and destroyed articular cartilage. Traditional treatments for OA are limited to alleviating various OA symptoms. There is a lack of drugs available in clinical practice that can truly repair cartilage damage. Here, we developed the chondroitin sulfate analog CS-semi5, semi-synthesized from chondroitin sulfate A. &lt;i>In vivo&lt;/i>, CS-semi5 alleviated inflammation, provided analgesic effects, and protected cartilage in the modified Hulth OA rat model and papain-induced OA rat model. A bioinformatics analysis was performed on samples from OA patients and an exosome analysis on papain-induced OA rats, revealing miR-122-5p as the key regulator associated with CS-semi5 in OA treatment. Binding prediction revea</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Aug</publication><modification>2026-07-15T10:58:16.082Z</modification><creation>2024-10-16T14:22:55.968Z</creation></dates><accession>S-EPMC11365380</accession><cross_references><pubmed>39220883</pubmed><doi>10.1016/j.apsb.2024.05.016</doi></cross_references></HashMap>