Chinese Patent Medicine Nei-Xiao-Pian Shrinks Thyroid Nodules by Regulating Proliferation and Apoptosis of Cells via Inhibiting the IL-6/JAK2/STAT3 Signaling Pathway.

BACKGROUND

Thyroid nodules (TN) are distinct lesions within the thyroid gland that can cause compression symptoms, disrupt thyroid function, and impact aesthetics and daily life. Nei-Xiao-Pian (NXP), a traditional Chinese patent medicine developed by Suzhou Hospital of Traditional Chinese Medicine, has been effectively used in clinical treatment for TN. Due to the complex nature of traditional Chinese medicine (TCM), limited clinical research exists on NXP, and its precise mechanisms of action remain largely unknown.

METHODS

In this study, we investigated the effects of NXP on human tumorous thyroid cells and papillary thyroid carcinoma (PTC) cells. Cells were treated with animal serum containing different concentrations of NXP. Cell viability, cell cycle progression, and apoptosis were assessed using the CCK-8 assay and flow cytometry. A literature review was also conducted to understand the physiological and pathological mechanisms underlying TN. Furthermore, we examined the involvement of the IL6/JAK2/STAT3 signaling pathway in the action of NXP by measuring the protein expression levels of IL-6, JAK2, and STAT3 in PTC cells using western blotting.

RESULTS

The present study showed that serum with a specific concentration of NXP reduced the viability of both tumorous thyroid cells and PTC cells, inhibited the proliferation of tumorous thyroid cells, and induced apoptosis. While NXP-containing serum did not significantly affect the cell cycle in PTC cells, it induced apoptosis in a dose-dependent manner. Additionally, NXP-containing serum dose-dependently suppressed the protein expressions of IL-6, JAK2, and STAT3 in PTC cells.

DISCUSSION: This study shows NXP-containing serum reduces thyroid tumor and PTC cell viability, inhibits proliferation, induces apoptosis (dose-dependent in PTC). It suppresses IL-6/JAK2/STAT3 in PTC, suggesting anti-tumor potential via this pathway, needing in vivo validation.

CONCLUSION

Our findings suggest that NXP may exert its therapeutic effects on TN by targeting the IL6/JAK2/STAT3 signaling pathway, thereby slowing disease progression. These results highlight a potential mechanism through which NXP could contribute to tumor prevention and treatment, offering a promising direction for future research.