PMID- 31667906 OWN - NLM STAT- MEDLINE DCOM- 20200430 LR - 20211204 IS - 1099-1573 (Electronic) IS - 0951-418X (Linking) VI - 34 IP - 2 DP - 2020 Feb TI - Bilobalide alleviates tumor necrosis factor-alpha-induced pancreatic beta-cell MIN6 apoptosis and dysfunction through upregulation of miR-153. PG - 409-417 LID - 10.1002/ptr.6533 [doi] AB - Type 1 diabetes mellitus (T1DM) is a systemic disease and one classical type of total DM. Bilobalide (BB) is constituted of EGb 761. Our purpose was identifying the role of BB in TIDM in the current study. MIN6 cells were treated by TNF-alpha; then, viability, apoptosis, and insulin secretion were assessed by performing Cell Counting Kit-8 assay, flow cytometry, glucose-stimulated insulin secretion assay, and western blot. The effects of BB were assessed to identify its function. Further, the above mentioned parameters were reassessed when silencing miR-153. TNF-alpha declined viability and insulin secretion as well as raised apoptosis and inducible nitric oxide synthase (iNOS) expression in MIN6 cells. BB alleviated the apoptosis and dysfunction induced by TNF-alpha. MiR-153 expression was elevated by BB when induced by TNF-alpha. Increase of viability and insulin secretion as well as decline of apoptosis and iNOS induced by BB treatment was alleviated by silencing miR-153. The rates of p/t-p70S6K, p/t-mammalian target of rapamycin (mTOR) and p/t-adenosine monophosphate-activated protein kinase (AMPK) were raised by BB and suppressed by silencing miR-153 under TNF-alpha induced condition. BB raised viability and insulin secretion, declined apoptosis and iNOS expression by up-regulating miR-153. Furthermore, BB activated AMPK/mTOR pathway by up-regulating miR-153. CI - (c) 2019 John Wiley & Sons, Ltd. FAU - Hao, Yan AU - Hao Y AD - Department of Endocrinology, Jining No.1 People's Hospital, Jining, China. FAU - Wang, Weiwei AU - Wang W AD - Department of Endocrinology, Jining No.1 People's Hospital, Jining, China. FAU - Wu, Dong AU - Wu D AD - Emergency Department, Jining No.1 People's Hospital, Jining, China. FAU - Liu, Kai AU - Liu K AD - Emergency Department, Jinxiang People's Hospital, Jining, China. FAU - Sun, Yihan AU - Sun Y AUID- ORCID: 0000-0001-6717-4898 AD - Department of Endocrinology, Jining No.1 People's Hospital, Jining, China. LA - eng PT - Journal Article PT - Retracted Publication DEP - 20191031 PL - England TA - Phytother Res JT - Phytotherapy research : PTR JID - 8904486 RN - 0 (Cyclopentanes) RN - 0 (Furans) RN - 0 (Ginkgolides) RN - 0 (Insulin) RN - 0 (MIRN153 microRNA, mouse) RN - 0 (MicroRNAs) RN - 0 (Tumor Necrosis Factor-alpha) RN - EC 1.14.13.39 (Nitric Oxide Synthase Type II) RN - EC 1.14.13.39 (Nos2 protein, mouse) RN - EC 2.7.1.1 (mTOR protein, mouse) RN - EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) RN - M81D2O8H7U (bilobalide) SB - IM RIN - Phytother Res. 2020 Oct;34(10):2778. PMID: 33051935 MH - Animals MH - Apoptosis/*drug effects MH - Cell Line, Tumor MH - Cyclopentanes/*pharmacology MH - Furans/*pharmacology MH - Ginkgolides/*pharmacology MH - Insulin/*analysis MH - Mice MH - MicroRNAs/*metabolism MH - Nitric Oxide Synthase Type II/metabolism MH - Ribosomal Protein S6 Kinases, 70-kDa/metabolism MH - Signal Transduction/drug effects MH - TOR Serine-Threonine Kinases/metabolism MH - Transcriptional Activation MH - Tumor Necrosis Factor-alpha/adverse effects MH - Up-Regulation OTO - NOTNLM OT - AMPK/mTOR pathway OT - apoptosis OT - diabetes mellitus (DM) OT - dysfunction EDAT- 2019/11/02 06:00 MHDA- 2020/05/01 06:00 CRDT- 2019/11/01 06:00 PHST- 2019/05/14 00:00 [received] PHST- 2019/09/22 00:00 [revised] PHST- 2019/10/09 00:00 [accepted] PHST- 2019/11/02 06:00 [pubmed] PHST- 2020/05/01 06:00 [medline] PHST- 2019/11/01 06:00 [entrez] AID - 10.1002/ptr.6533 [doi] PST - ppublish SO - Phytother Res. 2020 Feb;34(2):409-417. doi: 10.1002/ptr.6533. Epub 2019 Oct 31.