4.5 Article

BGM, a Newly Synthesised Boron Compound, Induces Apoptosis and Reduces Oxidative Stress by Inhibiting Lipogenesis in 3T3-L1 Adipocytes via PPARγ and CTRP3

期刊

BIOLOGICAL TRACE ELEMENT RESEARCH
卷 200, 期 11, 页码 4807-4816

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SPRINGERNATURE
DOI: 10.1007/s12011-022-03261-z

关键词

3T3-L1 adipocyte cells; Boron glycine mono-ester; CTRP3; PPAR gamma y; Apoptosis; Oxidative stress

资金

  1. National Boron Institute (BOREN) [2020-30-06-30-002]

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Obesity is a chronic disease with significant health implications, but there are limited treatment options available. This study investigated the anti-adipogenic activity of a newly synthesised compound called boron glycine monoester (BGM) and found that it has the potential to regulate adipogenesis and lipogenesis, as well as affect oxidative metabolism and apoptosis in adipocyte cells.
Obesity is a chronic disease associated with increased morbidity and mortality. The rapidly increasing prevalence of obesity makes it a global health problem, while treatment options remain limited. Given the potential of boron in the treatment of obesity, the aim of this study is to investigate the anti-adipogenic activity of the newly synthesised boron glycine monoester compound (BGM) using 3T3-L1 adipocytes by analysing lipid accumulation, CTRP3 and PPARy gene expression, oxidative stress and apoptotic effects. 3T3-L1 fibroblast cells (ATCC (R) CL-173) were transformed into adipocyte cells in vitro. Fat accumulation in the 3T3-L1 adipocyte cells was detected by Oil Red 0 staining. Gene expression levels were determined with qPCR. Biochemical analyzes were performed using spectrophotometric method (CAT, ALP and ACP) and ELISA kit (TAS, TOS, NADP-IDH). Apoptosis studies were performed on the muse cell nalyser using the Muse Annexin V & Dead Cell Assay Kit. When BGM-treated cells were compared to control adipocyte cells, lipid accumulation decreased in a dose-dependent manner. BGM-treated adipocyte cells had higher CTRP3 expression levels and lower PPAR-gamma gene expression levels compared to control adipocyte cells (p < 0.001). While BGM application increased the TAS level, it showed an antioxidant effect by regulating the activity of oxidative metabolism enzymes (p < 0.001). BGM application increased total apoptosis by 1.5-fold. These results show that BGM is a potential therapeutic agent for obesity by regulating the expression of genes related to adipogenesis and lipogenesis in adipocyte cells and by affecting the activity of enzymes of oxidative metabolism and apoptosis.

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