{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T16:56:27Z","timestamp":1790096187531,"version":"4.0.1"},"reference-count":39,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2024,9,4]],"date-time":"2024-09-04T00:00:00Z","timestamp":1725408000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Kaohsiung J of Med Scie"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>This study aims to investigate the effects of the Galectin\u20103 (Gal\u20103) inhibitor TD139 on inflammation and the extracellular signal\u2010regulated kinase (ERK)\/c\u2010Jun N\u2010terminal kinase (JNK)\/p38 pathway in gestational diabetes mellitus (GDM). Human placental tissues were treated with TD139 and TNF\u2010\u03b1, assessing Gal\u20103, ERK\/JNK\/p38 activation, and inflammatory cytokines. GDM was induced in mice via subcutaneous injections of streptozotocin (STZ). After confirming GDM, mice were treated with 15\u2009mg\/kg TD139 on GD 10.5 12.5, 14.5, 16.5, and 18.5. Serum inflammatory cytokines were measured on GD 20.5, and post\u2010delivery placental tissues were analyzed. Data were analyzed using one\u2010way or two\u2010way repeated measures ANOVA with post hoc tests. TD139 suppressed TNF\u2010\u03b1\u2010induced increases in Gal\u20103, IL\u20101\u03b2, IL\u20106, MCP\u20101, and ERK\/JNK\/p38 activation in placental tissues. In STZ\u2010induced GDM mice, TD139 reduced glucose levels, weight loss, and food and water intake. TD139 significantly lowered TNF\u2010\u03b1, IL\u20101\u03b2, IL\u20106, and MCP\u20101 in serum and placental tissues and inhibited the ERK\/JNK\/p38 pathway. TD139 improved pup numbers in GDM mice compared to untreated ones. TD139 reduces inflammation and inhibits the ERK\/JNK\/p38 pathway in TNF\u2010\u03b1 stimulated placental tissues and STZ\u2010induced GDM mice, suggesting its therapeutic potential for managing GDM\u2010related placental inflammation and improving pregnancy outcomes. The study used TNF\u2010\u03b1 to mimic GDM in placental tissues and an STZ\u2010induced GDM mouse model, which may not fully represent human GDM complexity. Future research should explore alternative models, and broader signaling pathways, and thoroughly evaluate TD139's safety in pregnancy.<\/jats:p>","DOI":"10.1002\/kjm2.12890","type":"journal-article","created":{"date-parts":[[2024,9,4]],"date-time":"2024-09-04T10:05:29Z","timestamp":1725444329000},"page":"916-925","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["<i>In vitro<\/i>\n                    and\n                    <i>in vivo<\/i>\n                    effects of Galectin\u20103 inhibitor\n                    <scp>TD139<\/scp>\n                    on inflammation and\n                    <scp>ERK<\/scp>\n                    \/\n                    <scp>JNK<\/scp>\n                    \/p38 pathway in gestational diabetes mellitus"],"prefix":"10.1002","volume":"40","author":[{"given":"Ji","family":"Xia","sequence":"first","affiliation":[{"name":"Department of Obstetrics, Hainan Branch, Shanghai Children's 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