{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,25]],"date-time":"2026-07-25T09:47:38Z","timestamp":1784972858209,"version":"3.55.0"},"reference-count":39,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2018,7,30]],"date-time":"2018-07-30T00:00:00Z","timestamp":1532908800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2018,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Baicalin (BAI), one major flavonoid from <jats:italic>Scutellaria baicalensis<\/jats:italic>, possesses anticancer and anti\u2010inflammatory properties. However, the effect of BAI on diabetes mellitus has not been investigated. This study explored the antidiabetic effect of BAI on pancreatic \u03b2\u2010cell line Min6. Min6 cells were treated with tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) to mimic \u03b2\u2010cell destruction in type 1 diabetes mellitus. The effects of BAI on viability and apoptosis of Min6 cells were analyzed by the cell counting kit\u20108 assay and Annexin V\u2010fluoresceine isothiocyanate\/propidium iodide staining method. The insulin secretion of Min6 cells was determined using radioimmunoassay. Expression of apoptosis\u2010associated proteins and inducible nitric oxide synthase (iNOS), and activation of phosphatidylinositol 3\u02b9\u2010kinase\/protein kinase B (PI3K\/AKT) and nuclear factor \u039aB (NF\u2010\u03baB) pathways were analyzed by Western blot analysis. Relative microRNA\u2010205 (miR\u2010205) expression was determined by quantitative real time polymerase chain reaction. TNF\u2010\u03b1 treatment inhibited cell growth and insulin secretion, but promoted iNOS expression. All of these effects were reversed by BAI treatment. BAI promoted viability; suppressed apoptosis; regulated caspase\u20103, B\u2010cell lymphoma 2 and Bcl\u20102\u2010associated X protein; decreased iNOS level; and increased insulin production. BAI protected Min6 cells by upregulating miR\u2010205. Besides, the Min6 cell\u2010protective effect of BAI was PI3K\/AKT pathway and NF\u2010\u03baB pathway dependent. BAI activated the PI3K\/AKT pathway and inhibited the NF\u2010\u03baB pathway by regulating miR\u2010205. In conclusion, BAI protected Min6 cells from TNF\u2010\u03b1\u2010induced injury by upregulating miR\u2010205, which acts, at least in part, via activation of the PI3K\/AKT pathway and inactivation of the NF\u2010\u03baB pathway.<\/jats:p>","DOI":"10.1002\/jcb.27095","type":"journal-article","created":{"date-parts":[[2018,7,30]],"date-time":"2018-07-30T07:56:16Z","timestamp":1532937376000},"page":"8547-8554","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["<i>Retracted<\/i>: Baicalin prevents tumor necrosis factor\u2010\u03b1\u2212induced apoptosis and dysfunction of pancreatic \u03b2\u2010cell line Min6 via upregulation of miR\u2010205"],"prefix":"10.1002","volume":"119","author":[{"given":"Wenjun","family":"You","sequence":"first","affiliation":[{"name":"Department of Endocrinology The Affiliated Hospital of Qingdao University  Qingdao Shandong China"},{"name":"Department of Endocrinology Jining No.1 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