Acute kidney injury (AKI) is the most common complication of sepsis with a high mortality rate. In this study, we focus on the renal injury caused by the immune response of renal tubular epithelial cells and inflammation-induced renal tubular epithelial cell apoptosis. We studied the role of GRP120 in the inflammation and apoptosis of human renal cell line HK-2 and mouse primary renal tubular epithelial cells. GPR120 agonist GW9508 activated the GPR120 pathway. Inflammatory factors were detected using quantitative real-time PCR and enzyme-linked immunosorbent assay. Cell apoptosis experiments included the annexin V and PI double-staining method combined with flow cytometry, TUNEL method, and Western blot. The level of cytokines including TNF-α, IL-6, IL-1β, and iNOS was significantly decreased (P < 0.05) in HK-2 and TECs after the activation of the GPR120 pathway. Besides, the cell apoptosis of both cells increased. Overexpressed GPR120 and shGPR120 were established. Treatment with lipopolysaccharide (LPS) increased the level of cytokines including TNF-α, IL-6, IL-1β, and iNOS in HK-2 cell and TECs. Compared with control-LPS and negative control (NC)-LPS, the overexpression of GPR120 and shGPR120 could decrease and increase the level of secreted cytokines significantly (P < 0.05), respectively, after LPS-induced apoptosis. After H₂O₂- and LPS-induced apoptosis, respectively, compared with the control and NC groups, overexpressed GPR120 and shGPR120 could reduce and increase the expression of caspase-3, respectively. GPR120 could suppress the cellular immune response and apoptosis in renal tubular epithelial cells, thereby possibly protecting the kidney and relieving sepsis-induced AKI.

急性肾损伤（AKI）是脓毒症最常见的并发症，死亡率高。在本研究中，我们重点关注肾小管上皮细胞的免疫反应和炎症诱导的肾小管上皮细胞凋亡引起的肾损伤。我们研究了 GRP120 在人肾细胞系 HK-2 和小鼠原代肾小管上皮细胞的炎症和凋亡中的作用。GPR120 激动剂 GW9508 激活 GPR120 通路。使用实时定量 PCR 和酶联免疫吸附试验检测炎症因子。细胞凋亡实验包括膜联蛋白V和PI双染法结合流式细胞术、TUNEL法和Western blot。TNF-α、IL-6、IL-1β、iNOS等细胞因子水平显着降低（P < 0.05) 在 GPR120 通路激活后 HK-2 和 TECs 中。此外，两种细胞的细胞凋亡均增加。建立了过表达的 GPR120 和 shGPR120。脂多糖 (LPS) 处理增加了 HK-2 细胞和 TECs 中细胞因子的水平，包括 TNF-α、IL-6、IL-1β 和 iNOS。与对照-LPS 和阴性对照 (NC)-LPS 相比 ，在 LPS 诱导细胞凋亡后，GPR120 和 shGPR120 的过表达可分别显着降低和增加分泌细胞因子的水平（P < 0.05）。H ₂ O _{2 后}- 和 LPS 诱导的细胞凋亡，分别与对照组和 NC 组相比，过表达 GPR120 和 shGPR120 可分别降低和增加 caspase-3 的表达。GPR120 可以抑制肾小管上皮细胞的细胞免疫反应和凋亡，从而可能保护肾脏并缓解脓毒症引起的 AKI。