【目的】 观察野黄芩苷调节磷脂酰肌醇-3激酶（PI3K）/蛋白激酶B（Akt）/核因子kappa B（NF-κB）信号通路对溃疡性结肠 炎小鼠结肠炎症损伤的影响。【方法】 以葡聚硫酸钠（DSS）诱导建立溃疡性结肠炎（UC）小鼠模型。将造模成功的小鼠随机分为 模型组、野黄芩苷组、YS-49（PI3K激活剂）组、野黄芩苷 + YS-49组，每组12只；另取12只BALB/c小鼠设为正常组。各组 给予相应干预后，对各组小鼠结肠炎症状进行疾病活动指数（DAI）评分，采用苏木精-伊红（HE）染色法观察各组小鼠结肠炎 症损伤症状并进行评分，伊文思蓝（EB）法测定各组小鼠肠道通透性，酶联免疫吸附分析（ELISA）法检测血清结肠损伤标志物 肠型脂肪酸结合蛋白（I-FABP）、二胺氧化酶（DAO）与促炎因子白细胞介素（IL）-1β、IL-17、肿瘤坏死因子α（TNF-α）水平， Western Blot 法检测结肠组织炎性因子 IL-1β、IL-17、TNF-α 与 PI3K/Akt/NF-κB 通路蛋白表达。【结果】 模型组小鼠 DAI 评 分，结肠炎症评分，肠壁EB含量，血清I-FABP与DAO水平，血清IL-1β、IL-17与TNF-α含量，结肠组织IL-1β、IL-17与 TNF-α蛋白表达水平，结肠组织p-PI3K/PI3K、p-Akt/Akt、p-NF-κB p65/NF-κB p65比值较正常组显著升高，差异均有统计 学意义（P < 0.05）。野黄芩苷组小鼠DAI评分，结肠炎症评分，肠壁EB含量，血清I-FABP与DAO水平，血清IL-1β、IL-17与 TNF-α含量，结肠组织IL-1β、IL-17与TNF-α蛋白表达水平，结肠组织p-PI3K/PI3K、p-Akt/Akt、p-NF-κB p65/NF-κB p65 比值较模型组降低，差异均有统计学意义（P < 0.05）；YS-49组小鼠DAI评分，肠壁EB含量，血清I-FABP与DAO水平，结 肠炎症评分，血清 IL-1β、IL-17与 TNF-α含量，结肠组织 IL-1β、IL-17与 TNF-α蛋白表达水平，结肠组织 p-PI3K/PI3K、 p-Akt/Akt、p-NF-κB p65/NF-κB p65较模型组升高，差异均有统计学意义（P < 0.05）。野黄芩苷+YS-49组小鼠DAI评分，肠 壁EB含量，血清I-FABP与DAO水平，结肠炎症评分，血清IL-1β、IL-17与TNF-α含量，结肠组织IL-1β、IL-17与TNF-α 蛋白表达水平，结肠组织p-PI3K/PI3K、p-Akt/Akt、p-NF-κB p65/NF-κB p65比值较野黄芩苷组升高，差异均有统计学意义 （P < 0.05）。【结论】 野黄芩苷可通过抑制PI3K/Akt/NF-κB信号通路激活减轻UC小鼠体内炎症，缓解其结肠炎症损伤并修复 肠道屏障功能。

Objective To observe the effect of scutellarin on colonic inflammatory injury in mice with ulcerative colitis by regulating phosphatidylinositol-3 kinase（PI3K）/protein kinase B（Akt）/nuclear factor kappa B（NF-κB） signaling pathway. Methods Ulcerative colitis（UC）mouse model was induced by dextran sulfate sodium（DSS）. The successfully modeled mice were randomly divided into model group， scutellarin group， YS-49（PI3 K activator）group and scutellarin + YS-49 group，with 12 mice in each group. Another 12 BALB/c mice were set as normal group. After the corresponding intervention was given to each group，the disease activity index（DAI）of colitis symptoms in each group was scored. Hematoxylin-eosin（HE）staining was used to observe and score the symptoms of colonic inflammatory injury in each group. Evans blue（EB）assay was used to determine the intestinal permeability of mice in each group. Enzyme-linked immunosorbent assay（ELISA）was used to detect the levels of serum colonic injury markers intestinal fatty acid binding protein（I-FABP）， diamine oxidase（DAO）and proinflammatory factors interleukin（IL）-1β，IL-17 and tumor necrosis factor α（TNF-α）. Western Blot was used to detect the expression of inflammatory factors IL-1β，IL-17，TNF-α and PI3K/Akt/NF-κB pathway proteins in colon tissue. Results The DAI score，colon inflammation score，EB content of intestinal wall，serum I-FABP and DAO levels，serum IL-1β，IL-17 and TNF-α levels，protein expression levels of colon tissue IL-1β，IL-17 and TNF -α，colon tissue p-PI3K/ PI3K，p-Akt/Akt，p-NF -κB p65/NF -κB p65 ratios in the model group were significantly higher than those in the normal group，and the differences were statistically significant（P < 0.05）. The DAI score，colon inflammation score，EB content in intestinal wall，serum I-FABP and DAO levels，serum IL-1β，IL-17 and TNF-α levels，protein expression levels of colon tissue IL-1β，IL-17 and TNF-α，colon tissue p-PI3 K/PI3 K，p-Akt/Akt，p-NF-κB p65/NF-κB p65 ratios in the scutellarin group were lower than those in the model group，and the differences were statistically significant（P < 0.05）. The DAI score，intestinal wall EB content，serum I-FABP and DAO levels，colon inflammation score，serum IL-1β，IL-17 and TNF-α levels， protein expression levels of colon tissue IL-1β，IL-17 and TNF-α，colon tissue p-PI3 K/PI3 K，p-Akt/Akt，p-NF- κB p65/NF-κB p65 in YS-49 group were higher than those in model group，and the differences were statistically significant（P < 0.05）. The DAI score， intestinal wall EB content， serum I-FABP and DAO levels， colonic inflammation score，serum IL-1β，IL-17 and TNF -α levels，protein expression levels of colon tissue IL-1β， IL-17 and TNF-α，colon tissue p-PI3K/PI3K，p-Akt/Akt，p-NF-κB p65/NF-κB p65 ratios in the scutellarin + YS-49 group were higher than those in the scutellarin group，and the differences were statistically significant（P < 0.05）. Conclusion Scutellarin can reduce inflammation in UC mice by inhibiting the activation of PI3K / Akt / NF - κB signaling pathway，alleviate colonic inflammatory injury and repair intestinal barrier function.

R285.5

武汉市中医药科研项目（编号：WZ22Z15）