PTGS1 (Prostaglandin-Endoperoxide Synthase 1)

Finally, a total of 70 potential drugs targeting these biomarkers were predicted. In conclusion, PTGS1 and PPBP were identified as key mitochondria-related genes associated with IDD, providing novel insights into the diagnosis and treatment of IDD.

Consistently, qPCR and Western blot analyses of mouse brain tissue homogenates revealed that DAO expression was significantly downregulated, whereas PTGS1, MMP8, MAPK14, and BCHE were significantly upregulated, consistent with computational predictions. These findings provide a novel molecular framework for understanding the link between environmental pollutants and mental disorders, confirming the neurotoxic effects of bisphenol compounds.

Additionally, increased MUC1 levels in circulating sEVs were confirmed by immunoassay (AUC = 0.840 for early-stage HGSOC vs HC; AUC = 0.860 for late-stage HGSOC vs HC, p-value<0.05). In summary, our sEV proteomic analysis of early-stage HGSOC reveals exo-biomarkers associated with early FT lesions, offering a promising avenue for detecting disease while it remains confined to the fallopian tube.

Western blot analysis further confirmed that KKP can effectively downregulate the expression of cytochrome P450 family 1 subfamily A member 1(CYP1A1), nitric oxide synthase 2(NOS2) and monoamine oxidase A(MAOA), arachidonate 5-lipoxygenase(ALOX5), prostaglandin-endoperoxide synthase 1(PTGS1), and p38 mitogen-activated protein kinase(p38 MAPK). In summary, the study reveals the clinical potential of KKP in the treatment of PIC and confirms that KKP alleviates inflammation and improves cough symptoms through multi-target and multi-pathway regulation, with the mechanism of action likely related to MAPK signaling pathway, arginine metabolism, and other inflammation-related pathways.

This study elucidates XLD's pleiotropic mechanisms in AMI management through network pharmacology approaches and identifies DA as a main active component XLD in alleviating AMI. These findings provide novel insights into XLD's cardioprotective pharmacology.

These findings confirm that canine SVF contains functional MSCs and possesses significant immunomodulatory and anti-proliferative capabilities against PBMCs, suggesting its therapeutic potential. This study also demonstrates coculture of SVF and PBMC as an in vitro model for studying therapeutic applications of stem cells in canine inflammatory and proliferative conditions.

Atrazine promotes CRC progression through multi-target and multi-pathway mechanisms. ABCC1 serves as the central gene linking Atrazine exposure to enhanced proliferation and migration of CRC cells.

Lymph node MSCs in DLBCL patients exhibit unique biological behavior and gene expression profiles, which may be closely related to clinical chemotherapy resistance.

Further in vitro experiments demonstrated that G-MDSCs may exert immunosuppressive functions through PTGS1 expression. Taken together, this study provides preliminary insights into the role of G-MDSCs in the MM TME and highlights potential therapeutic strategies to enhance CAR-T therapy efficacy, while acknowledging that larger and more diverse cohorts are required to substantiate these observations.

Taken together, the study clearly gave a comprehensive metabolic profile of DGJZD in vivo first. Our work reveals to study the material basis of the protective effects of DGJZD against GU and the underlying mechanisms.

Meanwhile, in vivo experiments with mice and transcriptome analysis demonstrated that the administration of LC extract had a beneficial impact on addressing HFD-induced hyperlipidemia induced by, particularly in regulating the genes ESR1, PPARG, and PTGS1/2. This study provides a scientific basis for LC compounds in the intervention of hyperlipidemia.

The integral components of BYXD are identified to selectively engage with a range of critical targets, modulating the associated signaling pathways that are pivotal in the pathophysiology of CHD. Such targeted modulation provides a substantive scientific basis for the clinical application of BYXD.