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Fabricated hydrogel composited membrane (HCM) is developed to reproduce the crystallization environment of monosodium urate monohydrate (MSUM) and then is equipped on a facile and versatile dynamic bionic platform to reveal the pathogenesis and control mechanism of gout after alcohol consumption. Especially, PEGDA/AA HCM can achieve the effective delay of MSUM nucleation and inhibition the crystals deposition (from 100% to 7.5%). [Display omitted] • Facile and versatile HCM based bionic platform was developed for gout control research. • Potential trigger mechanism of gout attack after alcohol intake was revealed. • PEGDA/AA HCM with abundant carboxylic acid groups effectively restrained MSUM crystallization. Gout is the most common of inflammatory arthropathy caused by the crystallization and accumulation of monosodium urate monohydrate (MSUM) in joints. Herein, fabricated hydrogel composited membrane (HCM) is developed to simulate the mass transfer in joints. A facile and versatile HCM based dynamic platform is established to investigate the "triggers" mechanism of gout under alcohol and its metabolites (acetaldehyde (AH) and acetic acid (HAc) intake condition. The distinct role of EtOH on enhanced gout onset was demonstrated, which attributes to the low interaction energy (E int) between EtOH and the main crystal surface. While, HAc and carboxyl groups exhibit potentially restrain the MSUM crystallization. This conclusion is furtherly confirmed by the different restraint performance of two kinds of fabricated HCM. PEGDA/AA (polyethylene glycol diacrylate/acrylic acid) with abundant carboxyl groups can delay the appearance time of MSUM crystals from 20 h to 82 h and reduce the crystal yield to 7.5% of the one via PEGDA/NIPAM (N-isopropylacrylamide). The excellent electronegativity of PEGDA/AA renders the adsorption of sodium ion on the HCM interface, which furtherly increases the nucleation energy barrier of MSUM crystal. The functional HCM based platform can guide the relevant biomedical research and rational drug design for gout prevention. [ABSTRACT FROM AUTHOR]