Plantamajoside improves type 2 diabetes mellitus pancreatic β-cell damage by inhibiting endoplasmic reticulum stress through Dnajc1 up-regulation

0303 health sciences 03 medical and health sciences
DOI: 10.4239/wjd.v16.i2.99053 Publication Date: 2024-12-30T02:12:23Z
ABSTRACT
Plantamajoside (PMS) has shown potential in mitigating cell damage caused by high glucose (HG) levels. Despite this, the precise therapeutic effects of PMS on type 2 diabetes mellitus (T2DM) and underlying regulatory mechanisms require further exploration. To investigate T2DM mice elucidate its action through vivo vitro experiments. An model MIN6 cells was established using HG palmitic acid (PA). PMS's protective effect assessed. Next, transcriptomics employed to examine how treatment affects gene expression cells. Furthermore, protein processing endoplasmic reticulum apoptosis pathways validated. A mouse used validate vivo. intervention ameliorated injury + PA-induced damage. Transcriptomic analysis revealed that were enriched treated with PMS, significant downregulation Dnajc1. Further validation indicated significantly inhibited apoptosis-related factors (Bax, CytC) stress (ERS)-related [ATF6, XBP1, Ddit3 (CHOP), GRP78], while promoting Bcl-2 Additionally, inhibitory ERS abolished upon Dnajc1 silencing. experiments demonstrated effectively improved pancreatic damage, suppressed CytC), ERS-related a mice. could alleviate tissue effectively. The mechanism involves activation, which subsequently inhibits ERS, ameliorating β-cells.
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