Wang Duo, Wang Yuan-Song, Zhao Hong-Min, Lu Peng, Li Meng, Li Wei, Cui Huan-Tian, Zhang Zhong-Yong, Lv Shu-Quan
Department of Endocrinology, Cangzhou Hospital of Integrated Traditional Chinese Medicine and Western Medicine of Hebei Province Affiliated to Hebei University of Chinese Medicine, Cangzhou 061000, Hebei Province, China.
Department of Endocrinology, Xianxian Hospital of Traditional Chinese Medicine of Hebei, Cangzhou 062250, Hebei Province, China.
World J Diabetes. 2025 Feb 15;16(2):99053. doi: 10.4239/wjd.v16.i2.99053.
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.
To investigate PMS therapeutic effects on T2DM in mice and elucidate its mechanisms of action through and experiments.
An 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 .
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, 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.
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 β-cells.
毛蕊花糖苷（PMS）已显示出减轻高糖（HG）水平引起的细胞损伤的潜力。尽管如此，PMS对2型糖尿病（T2DM）的确切治疗效果及其潜在的调节机制仍需进一步探索。
研究PMS对小鼠T2DM的治疗作用，并通过[具体实验]和[具体实验]阐明其作用机制。
使用HG和棕榈酸（PA）建立MIN6细胞的[具体损伤]模型。评估PMS对细胞损伤的保护作用。接下来，采用转录组学研究PMS处理如何影响MIN6细胞的基因表达。此外，验证了PMS对内质网蛋白加工和凋亡途径的影响。使用T2DM小鼠模型验证PMS的治疗效果和机制。
PMS干预改善了HG + PA诱导的MIN6细胞损伤中的细胞损伤。转录组分析显示，内质网蛋白加工和凋亡途径在PMS处理的细胞中富集，基因Dnajc1显著下调。进一步验证表明，PMS显著抑制凋亡相关因子（Bax、CytC）和内质网应激（ERS）相关因子[ATF6、XBP1、Ddit3（CHOP）、GRP78]的表达，同时促进Bcl-2和Dnajc1的表达。此外，Dnajc1沉默后，PMS对ERS和凋亡的抑制作用被消除。此外，[具体实验]表明，PMS干预有效改善了T2DM模型小鼠的胰腺损伤，抑制了凋亡相关因子（Bax、CytC）和ERS相关因子[ATF6、XBP1、Ddit3（CHOP）、GRP78]的表达，同时促进了Bcl-2和Dnajc1的表达。
PMS干预可有效减轻胰腺组织损伤。其作用机制涉及Dnajc1的激活，随后抑制凋亡和ERS，改善胰腺β细胞损伤。
