Polyelectrolyte Microcapsules Enhance the Stability of β-Galactosidase Under Simulated Gastrointestinal Conditions
TL;DR
MnCO3-templated PMCs effectively protect β-galactosidase from gastrointestinal degradation, sustain prolonged catalytic activity, and offer excellent storage stability, highlighting their strong potential for improving oral enzyme replacement therapy in lactose intolerance.
Abstract
Oral enzyme replacement therapy for lactase deficiency is limited by the rapid degradation of free β-galactosidase in the gastrointestinal tract. To overcome this, β-galactosidase was encapsulated into polyelectrolyte microcapsules (PMCs) via layer-by-layer assembly using MnCO3 sacrificial templates, with CaCO3-based PMCs as a reference. MnCO3-PMCs achieved 99.4% encapsulation efficiency and retained 85.8% of initial activity, significantly outperforming CaCO3-PMCs (86.0% and 29.7%). Under simulated gastric conditions (pH 2.0, pepsin), the free enzyme and CaCO3-PMCs were completely inactivated, whereas MnCO3-PMCs preserved ~86% activity. In simulated intestinal fluid, MnCO3-PMCs exhibited a 4.3-fold activity increase within the first hour and maintained a 2.5-fold enhancement after 70 h, while the free enzyme progressively inactivated. Furthermore, MnCO3-PMCs demonstrated superior storage stability, retaining 64% of initial activity after 90 days at 4 °C, compared with 25% for CaCO3-PMCs. Although immobilization increased the Michaelis constant, the shift was smaller for MnCO3-PMCs (8.9-fold) than for CaCO3-PMCs (15.2-fold). In conclusion, MnCO3-templated PMCs effectively protect β-galactosidase from gastrointestinal degradation, sustain prolonged catalytic activity, and offer excellent storage stability, highlighting their strong potential for improving oral enzyme replacement therapy in lactose intolerance.