Role of epigallocatechin gallate on aluminum exposure-induced bone damage via NLRP3 inflammasome signaling pathway.

BACKGROUND

Aluminum (Al) residue in the ecosystem has been increasing significantly, making Al exposure inevitable. Al has been shown to inhibit bone formation and cause osteoporosis. Epigallocatechin gallate (EGCG), which is one of the primary polyphenols found in green tea, has shown positive impacts on bone health; however, its possible therapeutic role in preventing Al-induced bone damage remains insufficiently explored. The study aimed to examine the effect of EGCG on Al-induced bone damage possibly through modulation of the NLRP3 inflammasome pathway.

METHODS

Rats were exposed to AlCl₃ to induce bone damage and treated with different doses of EGCG. Bone and serum mineral levels were determined using biochemical analyses. Relative mRNA expression levels of NLRP3, caspase-1, IL-1β, OPN, and OCN in bone tissue were evaluated by RT-PCR analysis and bone IL-1β levels were determined by ELISA.

RESULTS

AlCl3 exposure increased Al accumulation and serum Ca levels in rat bones, while decreasing bone Ca levels. It also induced bone damage through the activation of the NLRP3/caspase-1/IL-1β pathway. EGCG treatment resulted in dose-dependent recovery of these parameters. AlCl₃ exposure significantly increased OPN mRNA expression, while OCN mRNA expression showed a non-significant decreasing tendency. EGCG treatment was associated with reduced OPN mRNA expression and a tendency toward increased OCN mRNA expression.

CONCLUSIONS

These findings suggest that Al-induced bone damage may be associated with activation of the NLRP3 inflammasome pathway and that EGCG may exert protective effects, through modulation of this pathway. Thus, it was concluded that EGCG may be a promising protective agent for preventing Al-induced bone damage and may serve as a potential preventive agent for the treatment of bone diseases.