Carboxymethyl-β-cyclodextrin grafted chitosan embedded oyster (Crassostrea gigas) ferritin can alleviate lead-induced liver injury by oral administration.

Ferritin is expected to alleviate lead-induced oxidative damage. Despite being a relatively stable macromolecular protein that can withstand high temperatures and extreme pH conditions without its structure and activity being compromised, oral administration of ferritin may still result in its degradation within the gastrointestinal tract, reducing its bioavailability. In recent years, microcapsules have emerged as an effective approach in oral protein delivery to enhance bioavailability. In this study, carboxymethyl-β-cyclodextrin grafted chitosan embedded oyster (Crassostrea gigas) ferritin (CMCD-CS@GF1) was fabricated with favorable encapsulation efficiency (57.73 ± 4.84 %) and loading capacity (5.78 ± 0.48 %), as well as a certain degree of resistance to digestion in the gastric environment. In the simulated gastric fluid with an acidic pH, the cumulative release of GF1 over 4 h was 24.18 %. In the simulated intestinal fluid with a neutral pH, the cumulative release of GF1 over 8 h was 70.56 %. Animal experiments showed that oyster ferritin could reduce the accumulation of lead in the body, enhance the activity of antioxidant enzymes, activate the Nrf2 signaling pathway, and down-regulate the NLRP3 signaling pathway to reduce oxidative stress and inflammation levels. The findings demonstrate that oyster ferritin may mitigate the toxic effects of lead in the body, providing a significant theoretical foundation for its application in functional foods.