Curcumin (CCM) has many potential uses in anticancer chemotherapy, but its low water solubility poses a major problem, preventing its translation into clinical use. TPGS is a water-soluble derivative of vitamin E that acts as a surfactant with the ability to form micellar nanoparticles in water. More importantly, TPGS acts as a potent antioxidant that can neutralize intracellular reactive oxygen species (ROS). In this study, we solubilized CCM with TPGS using thin-film rehydration to prepare aqueous formulations containing CCM at clinically relevant concentrations. We found that the minimal TPGS:CCM ratio for producing nanoparticles was 5:1 (w/w): at or above this ratio, stable nanoparticles formed with an average particle diameter of 12 nm. CCM was released from TPGS/CCM micelles in simulated colonic and gastric fluids. These TPGS/CCM nanoparticles were shown to decrease intracellular ROS levels and apoptosis and inhibited migration of HT-29 human colon cancer cells more potently than free CCM. Pharmacokinetic analysis showed TPGS/CCM to be more bioavailable than free CCM after oral administration to rats. Our results suggest that TPGS/CCM may increase therapeutic efficacy of CCM against colon cancer and merits further investigation in a clinical setting.

Cerebral ischemia–reperfusion injury (CIRI) represents a major contributing factor to adverse outcomes following ischemic stroke (IS), posing signifi

Aflatoxin B1 (AFB1) is a highly toxic mycotoxin that causes severe renal injury, yet the molecular basis of its nephrotoxicity remains poorly defined. Here, we integrated multi-omics data with computational modeling to elucidate the mechanisms of AFB1-induced kidney damage. Three human renal transplant biopsy microarray datasets (GSE1563, GSE30718, and GSE61739), comprising 121 injury samples and 84 control samples and representing distinct forms of transplant-associated renal injury, including acute rejection and ischemic kidney injury, were analyzed using differential expression and weighted gene co-expression network analyses, which identified 174 injury-related genes. A total of 145 AFB1-associated targets were obtained from multiple public datasets. Intersection analysis between these two gene sets identified RXRB and F11 as core hub genes potentially involved in AFB1-induced renal injury. Immune infiltration and gene set enrichment analyses suggested their involvement in immune regulation and toxicity-related signaling pathways. Molecular docking demonstrated favorable binding of AFB1 to RXRB and F11, with binding energies of -9.9 and -7.4 kcal/mol, respectively, while molecular dynamics simulations further confirmed the stability of these complexes. Together, this integrative multi-omics and modeling approach reveals key molecular determinants of AFB1-induced renal toxicity and offers a theoretical foundation for developing targeted interventions against AFB1-related kidney disorders.