Green coffee bean extract (GCBE) supplements are widely marketed for weight management, primarily due to their chlorogenic acids (CGAs) and caffeine content. This study evaluated the authenticity and quality of 23 commercial GCBE products by quantifying three major CGA isomers (3-CQA, 4-CQA and 5-CQA) and caffeine using HPLC-DAD. The CGA content ranged from non-detectable to 31.15%, with 5-CQA being predominant. Caffeine levels varied from non-detectable to 3.82%. Notably, two samples labelled as containing 50% CGAs had none detected, while several 'decaffeinated' products exceeded regulatory caffeine thresholds. Only three samples declared caffeine levels, none of which were fully compliant with their labels. Hierarchical cluster analysis (HCA) grouped the supplements into four distinct clusters based on total CGA and caffeine content, revealing widespread inconsistencies. These findings raise concerns over mislabelling, regulatory non-compliance, and potential health risks, underscoring the urgent need for stricter quality control and accurate labelling in the dietary supplement industry.

2026-06-01·CELL DEATH AND DIFFERENTIATION

cGAS restricts PARP1-mediated microhomology-mediated end joining by suppressing poly-ADP-ribosylation

Article

作者: Li, Wenjing ; Zhu, Xueping ; Wu, Bo ; Gao, Boya ; Lan, Li ; Phoon, Laiyee ; Yang, Haibo ; Zhao, Weixing ; Luo, Jing ; Jia, Li ; Gui, Fu

Repair of DNA double-strand breaks (DSBs) is essential for cells to maintain genome stability and cell survival. While cyclic GMP-AMP synthase (cGAS) is best known for its role in innate immunity, emerging evidence reveals that it plays regulatory roles in DNA damage response. In this study, we demonstrate that cGAS suppresses PARP1-mediated poly(ADP-ribose) (PAR) formation at both double-stranded DNA (dsDNA) and DNA:RNA hybrids. As a result, cGAS deficiency enhances PARP1-mediated microhomology-mediated end joining (MMEJ). Since MMEJ competes with transcription-coupled homologous recombination (TC-HR) at actively transcribed genomic regions, cGAS-mediated suppression of MMEJ consequently leads to efficient TC-HR with increased recruitment of RAD52 and RAD51. Mechanistically, the zinc finger domain of cGAS binds PAR, inhibiting PARP1 activation. In prostate cancer cells, loss of cGAS increases dependency on PARP1, rendering them more sensitive to PARP inhibitors. Collectively, our findings uncover a noncanonical role for cGAS in negatively regulating PARP1-mediated MMEJ and suggest its potential as a therapeutic biomarker in prostate cancer.

2026-06-01·CYTOTECHNOLOGY

The role of pterostilbene in alleviating inflammatory response and pyroptosis in myocardial ischemia-reperfusion by inhibiting the cGAS-STING pathway

Article

作者: Zhu, Lingying ; Li, Hui ; He, Yongsheng ; He, Jigang ; Yan, Dan

Supplementary Information:

The online version contains supplementary material available at 10.1007/s10616-026-00976-y.

100 项与 cGAS(Twentyeight-Seven) 相关的药物交易

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