Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, 212000, P. R. China.
Center for Clinical Laboratories, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, 212000, P. R. China.
Int J Med Sci. 2022 Mar 21;19(4):631-639. doi: 10.7150/ijms.66167. eCollection 2022.
To elucidate the effect of Schistosoma japonicum peptide (SJMHE1) on pyroptosis in thyroid follicular epithelial cells (TFCs) induced by excessive iodine and the potential mechanism, the effects of SJMHE1 were investigated in NaI-treated Nthy-ori 3-1 cells; and the involvement of the ROS/MAPK/NF-κB signaling pathways in these effects was evaluated by employing CCK-8 assays, flow cytometry, ELISA, and Western blotting experiments. We found that SJMHE1 significantly reduced NLRP3, N-terminus of gasdermin D (GSDMD-N) and cleaved caspase-1 (C-caspase-1) expression, and decreased IL-1β secretion in TFCs. SJMHE1 also markedly reduced reactive oxygen species (ROS) production, and decreased the phosphorylation levels of MAPK and NF-κB pathway members. Moreover, blocking of the Toll-like receptor 2 significantly impaired SJMHE1-mediated protection from excessive iodine-induced pyroptosis in TFCs. Therefore, our results suggested a protective role of SJMHE1 in excessive iodine-induced pyroptosis in TFCs, which might be attributed to its suppression for ROS/MAPK/NF-κB signaling pathway by binding of SJMHE1 with TLR2.
为了阐明日本血吸虫肽（SJMHE1）对过量碘诱导的甲状腺滤泡上皮细胞（TFCs）细胞焦亡的影响及其潜在机制，本研究在 NaI 处理的 Nthy-ori 3-1 细胞中研究了 SJMHE1 的作用；并通过 CCK-8 测定、流式细胞术、ELISA 和 Western blot 实验评估了 ROS/MAPK/NF-κB 信号通路在此作用中的参与情况。我们发现 SJMHE1 可显著降低 NLRP3、gasdermin D（GSDMD-N）N 端和裂解的半胱天冬酶-1（C-caspase-1）的表达，并降低 TFCs 中 IL-1β的分泌。SJMHE1 还显著降低了活性氧（ROS）的产生，并降低了 MAPK 和 NF-κB 途径成员的磷酸化水平。此外，阻断 Toll 样受体 2 显著削弱了 SJMHE1 介导的对 TFCs 中过量碘诱导的细胞焦亡的保护作用。因此，我们的研究结果表明，SJMHE1 在 TFCs 中对过量碘诱导的细胞焦亡具有保护作用，这可能归因于 SJMHE1 通过与 TLR2 结合抑制了 ROS/MAPK/NF-κB 信号通路。
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