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目的 探讨姜黄素(Cur)对溃疡性结肠炎(UC)炎症的影响及其作用机制。方法 选取健康雄性C57BL/6小鼠，随机分为对照组、姜黄素组、2%葡聚糖硫酸钠(DSS)构建模型组、姜黄素治疗组，每组10只。HE染色法检测各组小鼠结肠组织病理学变化；TUNEL方法检测小鼠结肠上皮细胞凋亡情况；ELISA检测各组小鼠结肠组织中TNF-α、IL-6、MDA和SOD含量；免疫荧光检测各组小鼠结肠组织中NF-κBp65表达；Western blot检测各组小鼠结肠组织中NF-κB、Nrf2以及HO-1蛋白的表达情况。结果 姜黄素治疗可以改善模型小鼠的病理组织学变化，降低小鼠肠上皮细胞凋亡数量，降低小鼠结肠组织中TNF-α和IL-6的表达，降低MDA水平，上调SOD的水平；抑制小鼠NF-κBp65的表达，并阻止NF-κBp65转移到细胞核；提高Nrf2的表达，并促进Nrf2转移到细胞核；上调结肠组织中HO-1蛋白的表达。结论 姜黄素介导Nrf2/HO-1途径调节NF-κB核转移抑制氧化应激减轻溃疡性结肠炎炎症反应。
Abstract：Objective To investigate the effect and mechanism of curcumin(Cur)on inflammatory responses in ulcerative colitis(UC).Methods The healthy male C57BL/6 mice were selected and randomly divided into the control group, curcumin group, 2% dextran sulfate sodium(DSS)model construction group, and curcumin treatment group, with 10 mice in each group.The pathological changes in colonic tissues of mice were detected by HE staining.The apoptosis of colonic epithelial cells in mice was detected by the TUNEL method.The contents of TNF-α,IL-6,MDA and SOD in the colon tissues of mice were detected by ELISA.The expression of NF-κBp65 in the colon tissues of mice was detected by immunofluorescence.The expressions of NF-κB,Nrf2 and HO-1 in the colon tissues of mice were detected by Western blot.Results Curcumin treatment could improve the histopathological changes of model mice, reduce the number of apoptotic intestinal epithelial cells in mice, decrease the expressions of TNF-α and IL-6 in the colon tissue of mice, lower the level of MDA,and upregulate the level of SOD,inhibit the expression of NF-κBp65 in mice and prevent the transfer of NF-κBp65 to the nucleus, increase the expression of Nrf2 and promote the transfer of Nrf2 to the nucleus, up-regulate the expression of HO-1 in colon tissue of mice.Conclusion Curcumin ameliorates the inflammatory responses of ulcerative colitis by regulating the nuclear translocation of NF-κB through mediating activation of Nrf/HO-1 pathway to inhibit oxidative stress.
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基本信息:
DOI：10.16695/j.cnki.1006-2947.2026.02.001
中图分类号:R285.5
引用信息:
[1]杨帆,周生来,刘倩.姜黄素介导Nrf2/HO-1途径调节NF-κB核转移抑制氧化应激改善溃疡性结肠炎[J].解剖科学进展,2026,32(02):149-152+156.DOI:10.16695/j.cnki.1006-2947.2026.02.001.
基金信息:
辽宁省自然科学基金(20180550241)
2026-02-13
2026-02-13
2026-02-13