Anti-Inflammatory Regulatory Role of Signal Transducer and Activator of Transcription 3 Phosphorylation in Regulating Hypersensitivity Responses to Hydatid Cyst Fluid.

OBJECTIVE

This study aims to investigate the anti-inflammatory regulatory function of signal transducer and activator of transcription 3 (STAT3) phosphorylation in hypersensitivity responses triggered by hydatid cyst fluid through in vitro RBL-2H3 cell culture.

METHODS

RBL-2H3 cells were cultured in vitro and sensitized with immunoglobulin E (IgE), followed by intervention with STAT3 inhibitors Stattic and JSI-124. Cells were subsequently exposed to crude hydatid cyst fluid to induce an allergic reaction. β-Hexosaminidase (HEX) release in the cell supernatant was measured to evaluate degranulation. Apoptosis was detected using flow cytometry, and changes in phosphorylated protein levels were determined via Western Blot analysis.

RESULTS

Analysis of β-HEX release in the -induced IgE-mediated RBL-2H3 cell degranulation model revealed that both inhibitors effectively inhibited mast cell degranulation ( < 0.01). Apoptosis assays revealed that both inhibitors caused varying degrees of cell damage ( < 0.01), potentially leading to late-stage apoptosis.

CONCLUSION

Immunoblotting analyses confirmed that treatment with the two inhibitors reduced STAT3 phosphorylation levels at the S727 and Y705 sites, thereby inhibiting cell degranulation and alleviating immune responses.