基于AMPK/NLRP3通路探讨泽兰叶黄素对分泌性中耳炎大鼠的作用机制

doi:10.3969/j.issn.1006-6233.2025.10.012

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摘要 目的: 基于AMPK/NLRP3通路探讨泽兰叶黄素对分泌性中耳炎大鼠的影响,并初步探讨其可能的作用机制。方法: 将50只6-8周龄的大鼠随机分为对照组、模型组、泽兰叶黄素低剂量组(20mg/kg)、泽兰叶黄素高剂量组(80mg/kg)、泽兰叶黄素高剂量+AMPK抑制剂组(80mg/kg+20mg/kg),每组10只。通过注射内毒素构建分泌性中耳炎大鼠模型。造模成功后,泽兰叶黄素低剂量组,泽兰叶黄素高剂量组,泽兰叶黄素高剂量+AMPK抑制剂组以相应的药物进行腹腔注射,对照组和模型组则注射等体积生理盐水。HE染色用于观察中耳黏膜组织形态变化,测微计测量中耳黏膜厚度,ABR仪检测ABR反应阈值,酶联免疫吸附检测血清中炎症因子水平,实时荧光定量PCR检测各组IFN-γ和IL-4基因表达水平,Western Blot法检测大鼠黏膜组织中AMPK/NLRP3通路相关蛋白表达。结果: 与对照组相比,模型组中耳黏膜组织病理损伤程度加重,中耳黏膜厚度、ABR反应阈值、炎症因子水平、NLRP3蛋白表达升高(P<0.05),而IFN-γ/IL-4比值水平、p-AMPK蛋白表达降低(P<0.05)。与模型组相比泽兰叶黄素低剂量组和泽兰叶黄素高剂量组中耳黏膜组织病理损伤程度减轻,中耳黏膜厚度、ABR反应阈值、炎症因子水平、NLRP3蛋白表达降低(P<0.05),而IFN-γ/IL-4比值水平、p-AMPK蛋白表达升高(P<0.05)。与泽兰叶黄素高剂量组相比高剂量+AMPK抑制剂组的上述指标均被逆转(P<0.05)。结论: 泽兰叶黄素能显著改善分泌性中耳炎大鼠的炎症反应,其机制可能是通过激活AMPK通路,抑制NLRP3炎症小体活化,减少炎症因子的释放,从而减轻中耳黏膜组织损伤。

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	邓翔宇
	陈红兵

关键词 ：泽兰叶黄素, 分泌性中耳炎, AMPK, NLRP3

Abstract：Objective: To explore the impact of eupafolin on rats with secretory otitis media via the AMPK/NLRP3 pathway and preliminarily probe its potential mechanism. Methods: Fifty 6-8-week-old rats were randomly allocated into 5 groups: control, model, low-dose Eupolyphaga lutein (20mg/kg), high-dose Eupolyphaga lutein (80mg/kg), and high-dose Eupolyphaga lutein+AMPK inhibitor (80mg/kg + 20mg/kg), with 10 rats in each. Secretory otitis media rat models were established by endotoxin injection. Post-modeling, the low-, high-dose eupafolin and high-dose eupafolin+AMPK inhibitor groups received corresponding intraperitoneal drug injections, while the control and model groups got equal-volume saline. HE staining was used to observe middle ear mucosal tissue morphology; a micrometer, to measure its thickness; an ABR instrument, to detect the ABR response threshold; enzyme-linked immunosorbent assay, to test serum inflammatory factor levels; fluorescence quantitative PCR, to detect IFN-γ and IL-4 gene expression; and Western blot, to examine AMPK/NLRP3 pathway-related protein expression in rat mucosal tissue. Results: Compared to the control group, the model group had aggravated middle ear mucosal tissue pathology, increased thickness, ABR response threshold, inflammatory factor levels and NLRP3 protein expression (P<0.05), but decreased IFN-γ/IL-4 ratio and p-AMPK protein expression (P<0.05). Compared with the model group, the low- and high-dose eupafolin groups showed alleviated middle ear mucosal tissue pathology, reduced thickness, ABR response threshold, inflammatory factor levels and NLRP3 protein expression (P<0.05), while the IFN-γ/IL-4 ratio and p-AMPK protein expression were increased (P<0.05). Compared with the high-dose eupafolin group, the high-dose+AMPK inhibitor group had reversed the above indicators (P<0.05). Conclusion: Eupolyphaga lutein can markedly ameliorate the inflammatory response in rats with secretory otitis media. Its possible mechanism is activating the AMPK pathway, suppressing NLRP3 inflammasome activation, reducing inflammatory factor release, and thereby mitigating middle ear mucosal tissue damage.

Key words： Eupolyphaga lutein Secretory otitis media AMPK NLRP3

引用本文:

邓翔宇, 陈红兵. 基于AMPK/NLRP3通路探讨泽兰叶黄素对分泌性中耳炎大鼠的作用机制[J]. 河北医学, 2025, 31(10): 1657-1664.
DENG Xiangyu, CHEN Hongbing. The Mechanism of Lutein of Zephyr on Secretory Otitis Media Rats Based on AMPK/NLRP3 Pathway. HeBei Med, 2025, 31(10): 1657-1664.

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http://www.hbyxzzs.cn/CN/10.3969/j.issn.1006-6233.2025.10.012 或 http://www.hbyxzzs.cn/CN/Y2025/V31/I10/1657

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