Department of Gastroenterology, Daping Hospital, Army Medical University, Chongqing, PR China.
Department of Pathophysiology, High Altitude Military Medicine, Daping Hospital, Army Medical University, Chongqing, PR China.
Bioengineered. 2021 Dec;12(1):1436-1444. doi: 10.1080/21655979.2021.1920324.
The current study aimed to investigate the effects of sodium butyrate on the level of colonic protein IRAK1 (interleukin-1 receptor-associated kinase 1) in irritable bowel syndrome (IBS) models as well as revealing the relationship between IRAKI level and visceral sensitivity during the progression of IBS. IBS symptoms were induced using TNBS (2,4,6-trinitrobenzene sulfonic acid) in mice and using IL-33 in HT-29 cells, which were then hanlded with sodium butyrate (100 mM for each mice and 0.05 M for HT-29 cells). The threshold of visceral pain and the expression of IRAKI in mice, and the level of IRAKI in HT-29 cells were detected. The data showed that the level of IRAK1 in IBS mice was higher than that in the control group, while the pre-treatment with sodium butyrate could solidy suppressed the level of IRAK1. Morevoer, it was found that the level of IRAK1 was negatively correlated with the pain threshold. In in vitro assays, the level of IRAK1 was firstly induced by IL-33 stimulation and then suppressed by sodium butyrate pretreatment. Collectively, the level of IRAKI showed an obvioulty positive relation with visceral hypersensitivity in IBS models, and the treatment with sodium butyrate could alleviate visceral hypersensitivity by inhibiting the expression of IRAKI.
本研究旨在探讨丁酸钠对肠易激综合征（IBS）模型中结肠蛋白 IRAK1（白细胞介素-1受体相关激酶 1）水平的影响，并揭示 IRAK1 水平与 IBS 进展过程中内脏敏感性之间的关系。通过在小鼠中使用 TNBS（2,4,6-三硝基苯磺酸）和在 HT-29 细胞中使用 IL-33 诱导 IBS 症状，然后用丁酸钠（每只小鼠 100mM，HT-29 细胞 0.05M）处理。检测小鼠内脏疼痛阈值和 IRAK1 表达水平，以及 HT-29 细胞中 IRAK1 水平。结果表明，IBS 小鼠的 IRAK1 水平高于对照组，而丁酸钠预处理可显著抑制 IRAK1 水平。此外，还发现 IRAK1 水平与疼痛阈值呈负相关。在体外实验中，IL-33 刺激首先诱导 IRAK1 水平升高，然后丁酸钠预处理抑制 IRAK1 水平升高。综上所述，在 IBS 模型中，IRAK1 水平与内脏高敏性呈明显正相关，丁酸钠治疗可通过抑制 IRAK1 的表达缓解内脏高敏性。
