| 宋婷婷,柴瑞峰,杨春波,李 颖,李 建.NLRP3炎症小体对脓毒症大鼠肠道炎症与损伤及JAK/STAT3信号通路的影响[J].,2024,(13):2423-2427 |
| NLRP3炎症小体对脓毒症大鼠肠道炎症与损伤及JAK/STAT3信号通路的影响 |
| The Effects of NLRP3 Inflammasome on Intestinal Inflammatory, Injury and JAK/STAT3 Signaling Pathway in Septic Rats |
| 投稿时间：2023-11-20 修订日期：2023-12-13 |
| DOI：10.13241/j.cnki.pmb.2024.13.004 |
| 中文关键词: 脓毒症 炎症 核苷酸结合寡聚化结构域样受体蛋白3 JAK/STAT3信号通路 |
| 英文关键词: Sepsis Inflammation Nucleotide binding oligomerization domain like receptor protein 3 JAK/STAT3 signaling pathway |
| 基金项目:新疆维吾尔自治区自然科学基金项目（2021D01C306） |
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| 中文摘要: |
| 摘要 目的：探讨核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）炎症小体通过JAK/STAT3信号通路对脓毒症大鼠的肠道炎症反应和肠粘膜损伤的作用机制。方法：选择健康清洁级雄性Wistar大鼠30只， 随机分为三组：假手术组、模型组与NLRP3抑制剂组，各10只，模型组和抑制剂组采用盲肠结扎穿孔术进行造模，抑制剂组于造模前30 min腹腔注射NLRP3抑制剂MCC950（10 mg/kg），模型组注射等量生理盐水。观察各组大鼠24 h的生存情况，HE染色进行回肠病理评分，ELISA法检测血清肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β），Western blot法检测小肠组织 NF-κB p65、NLRP3、凋亡相关斑点蛋白（ASC）、天冬氨酸特异性半胱氨酸蛋白酶 1（Caspase-1）、p-JAK和p-STAT3蛋白表达量。结果：①与假手术组相比，模型组大鼠的死亡率和病理评分显著增加，血清TNF-α和IL-1β水平升高，组织 NF-κB p65、NLRP3、ASC、Caspase-1、p-JAK和p-STAT3蛋白的相对表达量均显著增加（P＜0.05）。②与模型组相比，抑制剂组大鼠的死亡率和病理评分显著降低，血清TNF-α和IL-1β水平，组织 NF-κB p65、NLRP3、ASC、Caspase-1、p-JAK和p-STAT3蛋白的表达量显著下降（P＜0.05）。抑制剂组与假手术组相比，上述指标间仍存在显著的统计学差异（P＜0.05）。结论：NLRP3炎症小体可能通过活化JAK/STAT3信号通路增强脓毒症大鼠的肠道炎症反应，损伤肠道黏膜，靶向干预NLRP3能够逆转肠道损伤。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the mechanism of nucleotides binding oligomeric domain like receptor protein 3 (NLRP3) inflammasome on the intestinal inflammatory response and intestinal mucosal injury in septic rats through the JAK/STAT3 signaling pathway. Methods: Thirty healthy and clean grade male Wistar rats were chosed and randomly divided into three groups: sham surgery group, model group, and NLRP3 inhibitor group, with 10 rats in each group. The model group and inhibitor group were subjected to cecal ligation and perforation for modeling. The inhibitor group was intraperitoneally injected with NLRP3 inhibitor MCC950 (10 mg/kg) 30 minutes before modeling, and the model group was injected with equal amount of physiological saline. The 24-hour survival status of rats in each group were observed, ileal pathological score was performed with HE staining, serum tumor necrosis factor-α(TNF-α) and interleukin-1β (IL-1β) were detected using ELISA method, NF-κB p65, NLRP3, apoptosis related spot protein (ASC), aspartate specific cysteine protease-1(Caspase-1), p-JAK, and p-STAT3 proteins levels in small intestine tissues were detected by Western blot method. Results: ① Compared with the sham surgery group, the mortality rate and pathological score of the model group rats significantly increased, serum TNF-α and IL-1β levels were higher, tissue NF-κB p65, NLRP3, ASC, Caspase-1, p-JAK, and p-STAT3 proteins relative expressions were significantly higher, too (P<0.05). ② Compared with the model group, the mortality rate and pathological score of the inhibitor group rats significantly reduced, serum TNF-α and IL-1β was significantly lower, levels of NF-κB p65, NLRP3, ASC, Caspase-1, p-JAK, and p-STAT3 proteins were significantly less, too(P<0.05). There were still significantly statistical differences between the inhibitor group and the sham surgery group in the above indicators (P<0.05). Conclusion: NLRP3 inflammasome may enhance the intestinal inflammatory response and injury intestinal mucosal in septic rats by activating JAK/STAT3 signaling pathway, targeting intervention of NLRP3 could reverse intestinal injury. |
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