Predicting molecular mechanism of silymarin-potentiated diclofenac toxicity: Insight from in silico molecular docking.

ABSTRACT: Silymarin was shown to enhance diclofenac toxicity by inducing the loss of mitochondrial membrane permeability (MMP) in Caco-2 cells, independent of endoplasmic reticulum stress. This study employed in silico molecular docking to further investigate the potential interaction between silymarin and specific mitochondrial proteins involved in the loss of mitochondria integrity, aiming to elucidate the underlying mechanism of potentiation. The target proteins for our docking analysis included mitochondrial complex I and III, voltage-dependent anion-selective channel (VDAC), and cyclophilin D (CypD). Our results indicated that diclofenac could bind to both mitochondrial complex I and III. In contrast, silymarin exhibited a strong interaction with mitochondrial complex I with the binding

SUBMITTER: Boonyong C 

PROVIDER: S-EPMC10582735 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature