机构：[1]Hebei Univ Chinese Med, Cangzhou Hosp Integrated Tradit Chinese Med & West, Dept Endocrinol, 31 West Yellow River Rd, Cangzhou 061000, Hebei, Peoples R China[2]Xianxian Hosp Tradit Chinese Med Hebei, Dept Endocrinol, Cangzhou 062250, Hebei, Peoples R China[3]Hebei Med Univ, Grad Sch, Shijiazhuang 050011, Hebei, Peoples R China[4]Hebei Univ Chinese Med, Grad Sch, Shijiazhuang 050299, Hebei, Peoples R China[5]Yunnan Univ Chinese Med, Sch Clin Med 1, Kunming 065000, Yunnan, Peoples R China
BACKGROUND 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 the underlying regulatory mechanisms require further exploration. AIM To investigate PMS therapeutic effects on T2DM in mice and elucidate its mechanisms of action through in vivo and in vitro experiments. METHODS An in vitro damage model of MIN6 cells was established using HG and palmitic acid (PA). PMS's protective effect on cell damage was assessed. Next, transcriptomics was employed to examine how PMS treatment affects gene expression of MIN6 cells. Furthermore, the effect of PMS on protein processing in endoplasmic reticulum and apoptosis pathways was validated. A T2DM mouse model was used to validate the therapeutic effects and mechanisms of PMS in vivo. RESULTS PMS intervention ameliorated cell injury in HG + PA-induced MIN6 cell damage. Transcriptomic analysis revealed that protein processing in the endoplasmic reticulum and apoptosis pathways were enriched in cells treated with PMS, with significant downregulation of the gene Dnajc1. Further validation indicated that PMS significantly inhibited the expression of apoptosis-related factors (Bax, CytC) and endoplasmic reticulum stress (ERS)-related factors [ATF6, XBP1, Ddit3 (CHOP), GRP78], while promoting the expression of Bcl-2 and Dnajc1. Additionally, the inhibitory effects of PMS on ERS and apoptosis were abolished upon Dnajc1 silencing. Furthermore, in vivo experiments demonstrated that PMS intervention effectively improved pancreatic damage, suppressed the expression of apoptosis-related factors (Bax, CytC), and ERS-related factors [ATF6, XBP1, Ddit3 (CHOP), GRP78], while promoting the expression of Bcl-2 and Dnajc1 in a T2DM model mice. CONCLUSION PMS intervention could alleviate pancreatic tissue damage effectively. The mechanism of action involves Dnajc1 activation, which subsequently inhibits apoptosis and ERS, ameliorating damage to pancreatic beta-cells.
基金：
Yuansong Wang National Famous Traditional Chinese Medicine Expert Heritage Studio, No. 4 (2022)
第一作者机构：[1]Hebei Univ Chinese Med, Cangzhou Hosp Integrated Tradit Chinese Med & West, Dept Endocrinol, 31 West Yellow River Rd, Cangzhou 061000, Hebei, Peoples R China
通讯作者：
推荐引用方式(GB/T 7714)：
Wang Duo,Wang Yuan-Song,Zhao Hong-Min,et al.Plantamajoside improves type 2 diabetes mellitus pancreatic β-cell damage by inhibiting endoplasmic reticulum stress through Dnajc1 up-regulation[J].WORLD JOURNAL OF DIABETES.2025,16(2):doi:10.4239/wjd.v16.i2.99053.
APA：
Wang, Duo,Wang, Yuan-Song,Zhao, Hong-Min,Lu, Peng,Li, Meng...&Lv, Shu-Quan.(2025).Plantamajoside improves type 2 diabetes mellitus pancreatic β-cell damage by inhibiting endoplasmic reticulum stress through Dnajc1 up-regulation.WORLD JOURNAL OF DIABETES,16,(2)
MLA：
Wang, Duo,et al."Plantamajoside improves type 2 diabetes mellitus pancreatic β-cell damage by inhibiting endoplasmic reticulum stress through Dnajc1 up-regulation".WORLD JOURNAL OF DIABETES 16..2(2025)
