Ulcerative colitis (UC) is a risk factor for carcinogenesis of colorectal cancer, which is associated with disruption of the epithelial barrier and disorder of the inflammatory response. It has been reported that the expression of microRNA (miR)-215 is upregulated in patients with long-term UC. The present study aimed to investigate the effects of miR-215 on lipopolysaccharide (LPS)-induced inflammatory injury in CCD-18Co cells, as well as to identify the underlying possible molecular mechanisms. CCD-18Co cells were treated with 1 µg/ml LPS to induce inflammatory injury. Reverse transcription-quantitative PCR was performed to determine the expression of miR-215 in LPS-treated CCD-18Co cells. Moreover, a dual luciferase reporter system assay was used to evaluate the interaction of miR-215 and growth differentiation factor 11 (GDF11) in CCD-18Co cells. The expression of miR-215 was significantly upregulated in LPS-treated CCD-18Co cells. Knockdown of miR-215 significantly alleviated the inflammatory response and oxidative stress in LPS-treated CCD-18Co cells. In addition, GDF11 was identified as a direct binding target of miR-215 in CCD-18Co cells. Knockdown of miR-215 significantly increased the expression of GDF11, but decreased the expression levels of Toll-like receptor (TLR)4, phosphorylated (p)-p65, iNOS, p-p38 and p-JNK in LPS-treated CCD-18Co cells. Collectively, the present findings indicated that knockdown of miR-215 alleviated oxidative stress and inflammatory response in LPS-treated CCD-18Co cells by upregulating GDF11 expression and inactivating the TLR4/NF-κB and JNK/p38 signaling pathways.

中文翻译：

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miR-215 的下调通过 TLR4/NF-kB 和 JNK/p38 信号通路靶向 GDF11，减轻脂多糖诱导的 CCD-18co 细胞炎症损伤。

溃疡性结肠炎（UC）是结直肠癌发生的危险因素，与上皮屏障的破坏和炎症反应的紊乱有关。据报道，长期 UC 患者中 microRNA (miR)-215 的表达上调。本研究旨在研究 miR-215 对脂多糖 (LPS) 诱导的 CCD-18Co 细胞炎症损伤的影响，并确定潜在的可能分子机制。CCD-18Co 细胞用 1 µg/ml LPS 处理以诱导炎症损伤。进行逆转录-定量 PCR 以确定 miR-215 在 LPS 处理的 CCD-18Co 细胞中的表达。而且，双荧光素酶报告系统测定用于评估 miR-215 和生长分化因子 11 (GDF11) 在 CCD-18Co 细胞中的相互作用。miR-215 的表达在 LPS 处理的 CCD-18Co 细胞中显着上调。敲除 miR-215 可显着减轻 LPS 处理的 CCD-18Co 细胞的炎症反应和氧化应激。此外，GDF11 被鉴定为 CCD-18Co 细胞中 miR-215 的直接结合靶点。敲低 miR-215 显着增加 GDF11 的表达，但降低了 LPS 处理的 CCD-18Co 中 Toll 样受体 (TLR)4、磷酸化 (p)-p65、iNOS、p-p38 和 p-JNK 的表达水平细胞。总的来说，