摘要： 目的 探讨PPAR-γ在高糖微环境下对人大细胞肺癌NCI-H460细胞增殖的影响及其分子机制。方法 分别用正常糖（空白组）、高渗（对照组）和30 mmol/L葡萄糖（高糖组）培养基处理NCI-H460细胞，用CCK-8法和平板克隆实验分析高糖微环境对NCI-H460细胞增殖能力的影响；用Western blotting检测NLRP3炎症小体相关蛋白和PPAR-γ蛋白的表达；用特异性PPAR-γ激活剂罗格列酮刺激高糖微环境下的NCI-H460细胞；用Western blotting检测NLRP3炎症小体相关蛋白的表达，CCK-8法和平板克隆实验分析高糖微环境下PPAR-γ对NCI-H460细胞增殖能力的影响；用NLRP3炎症小体激动剂NSS联合罗格列酮刺激高糖微环境下的NCI-H460细胞，CCK-8法和平板克隆实验分析NLRP3炎症小体是否参与高糖微环境下PPAR-γ对NCI-H460细胞增殖的抑制作用。结果 高糖微环境能够显著提高NCI-H460细胞的增殖能力，诱导NLRP3炎症小体活性升高，下调PPAR-γ蛋白表达，PPAR-γ激活剂罗格列酮能有效抑制NLRP3炎症小体的活性，抑制NCI-H460细胞的增殖，且这一作用可被NLRP3炎症小体激动剂逆转。结论 PPAR-γ通过下调NLRP3炎症小体活性，抑制高糖微环境下人大细胞肺癌NCI-H460细胞增殖。

PPAR-γ抑制高糖微环境下NCI-H460细胞增殖的分子机制

胡明亮

中国医科大学附属盛京医院胃肠营养外科, 沈阳 110004

收稿日期:2023-03-14出版日期:2023-12-30发布日期:2023-12-12
通讯作者:胡明亮E-mail:h583917717@163.com
作者简介:胡明亮(1986-),女,护师,本科
基金资助:辽宁省自然科学基金（2019-ZD-0739）


关键词: PPAR-γ, NLRP3炎症小体, 高糖微环境, 增殖, 人大细胞肺癌
Abstract: Objective To investigate the effect of PPAR-γ on the proliferation of human large cell lung cancer (NCI-H460) cells in a high-glucose microenvironment and to explore the associated molecular mechanism.Methods NCI-H460 cells were treated with normal-glucose (blank group), hypertonic (control group), and high-glucose (30 mmol/L; high-glucose group) media. The effects of a high-glucose microenvironment on the proliferation of NCI-H460 cells were analyzed using Cell Counting Kit 8 (CCK-8) and colony-formation assays. The specific PPAR-γ activator, rosiglitazone, was used to treat NCI-H460 cells in a high-glucose microenvironment, and the expression of NLRP3-inflammasome-related proteins was detected by western blotting. The effect of PPAR-γ on the proliferation of NCI-H460 cells in a high-glucose microenvironment was analyzed by CCK-8 and clony-formation assays. The NLRP3 inflammasome agonist, NSS, combined with rosiglitazone, were used to treat NCI-H460 cells in a high-glucose microenvironment. CCK-8 and clony-formation assays were used to analyze whether the NLRP3 inflammasome was involved in the inhibitory effect of PPAR-γ on the proliferation of NCI-H460 cells in a high-glucose microenvironment.Results A high-glucose microenvironment significantly induced the proliferation of NCI-H460 cells, increased the activity of the NLRP3 inflammasome, and reduced the expression levels of PPAR-γ protein. Rosiglitazone effectively inhibited NLRP3 inflammasome activity and NCI-H460 cell proliferation, and this effect was reversed by NLRP3 inflammasome agonist.Conclusion PPAR-γ inhibits the proliferation of NCI-H460 cells in a high-glucose microenvironment by down-regulating the activity of the NLRP3 inflammasome.
Key words: PPAR-γ, NLRP3 inflammasome, high-glucose microenvironment, proliferation, human large cell lung cancer
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