中成药内孝片通过抑制IL-6/JAK2/STAT3信号通路调节细胞增殖和凋亡收缩甲状腺结节

Yu-Ting Zhao, Yang Yang, Wen-Ting Mei, Ting Chen, Wei Wei, Yu-Chen Wu, Xiao Yu, Fei Huang
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引用次数: 0

摘要

背景:甲状腺结节(TN)是甲状腺内独特的病变,可引起压迫症状,破坏甲状腺功能,影响美学和日常生活。内孝片(NXP)是苏州中医院研发的中成药,已有效应用于TN的临床治疗。由于中药的复杂性,恩智浦的临床研究有限,其确切的作用机制仍不清楚。方法:研究恩智浦对人甲状腺肿瘤细胞和甲状腺乳头状癌(PTC)细胞的影响。用含有不同浓度恩智浦的动物血清处理细胞。采用CCK-8法和流式细胞术评估细胞活力、细胞周期进展和凋亡情况。此外,我们还进行了文献综述,以了解TN的生理和病理机制。此外,我们通过使用western blotting检测PTC细胞中IL-6、JAK2和STAT3的蛋白表达水平,研究了IL-6 /JAK2/STAT3信号通路在NXP作用中的作用。结果:本研究显示,特定浓度的恩智浦血清可降低甲状腺肿瘤细胞和PTC细胞的活力,抑制甲状腺肿瘤细胞的增殖,诱导细胞凋亡。含恩敏肽的血清对PTC细胞周期无显著影响,但诱导PTC细胞凋亡呈剂量依赖性。此外,含有nxp的血清剂量依赖性地抑制了PTC细胞中IL-6、JAK2和STAT3的蛋白表达。结论:我们的研究结果提示NXP可能通过靶向IL6/JAK2/STAT3信号通路来发挥其对TN的治疗作用,从而减缓疾病进展。这些结果突出了NXP对肿瘤预防和治疗的潜在机制,为未来的研究提供了一个有希望的方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

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.

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