目的 探讨和厚朴酚治疗溃疡性结肠炎（UC）的药效及机制。方法 将C57BL/6小鼠随机分为对照组、模型组、柳氮磺吡啶肠溶片（SASP，阳性药，0.6 g·kg^-1）及和厚朴酚高、低剂量（0.2、0.1 g·kg^-1）组，除对照组外，每组自由饮用3%葡聚糖硫酸钠（DSS）水溶液，连续5 d，建立UC模型，5 d后，按10 mL·kg^-1体积ig给药，对照组与模型组ig给予同体积纯净水，每天1次，连续给药6 d。观察小鼠一般情况，收集结肠长度、结肠质量长度比、脾脏指数和肠黏膜损伤指数（CMDI）评分数据；苏木素-伊红（HE）染色法观察结肠组织病理损伤； ELISA法检测血清中肿瘤坏死因子α（TNF-α）、白细胞介素（IL）-6、IL-1β、IL-10水平；免疫组化法检测结肠组织半胱天冬酶-3（Caspase-3）蛋白表达； Western blotting法检测结肠组织中磷脂酰肌醇3-激酶（PI3K）、p-PI3K、蛋白激酶B（Akt）、p-Akt蛋白表达；分子对接分析和厚朴酚与PI3K、Akt的结合效力。结果 与模型组比较，和厚朴酚作用于UC小鼠后，可显著增加结肠长度，降低结肠质量长度比、脾脏指数和CMDI评分（P＜0.01）；减轻组织病理损伤；显著降低TNF-α、IL-6、IL-1β的表达，显著升高IL-10的表达（P＜0.01）；显著降低Caspase-3、p-PI3K/PI3K、p-Akt/Akt的表达（P＜0.01）；分子对接结果显示和厚朴酚与PI3K、Akt具有较好的结合效力。结论 和厚朴酚可能通过抑制PI3K/Akt信号通路发挥对UC小鼠的保护作用。

Objective To investigate the pharmacodynamic effects and underlying mechanisms of honokiol in the treatment of ulcerative colitis (UC). Methods C57BL/6 mice were randomly divided into control, model, Sulfasalazine Enteric-Coated Tablets (SASP, positive drug, 0.6 g·kg^-1), and high- and low-dose honokiol groups (0.2 and 0.1 g·kg^-1). Except for the control group, all other groups were freely given 3% dextran sulfate sodium (DSS) solution for five consecutive days to establish the ulcerative colitis (UC) model. Five days after DSS administration, drugs were administered orally at a volume of 10 mL·kg^-1 once daily for six consecutive days. The control and model groups received an equal volume of pure water. General conditions of the mice were observed, and data on colon length, colon weight-to-length ratio, spleen index, and colonic mucosal damage index (CMDI) scores were collected. Histopathological changes in colonic tissues were examined using hematoxylin-eosin (HE) staining. Serum levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-1β, and IL-10 were measured by ELISA. Expression of caspase-3 protein in colonic tissues was detected by immunohistochemistry. Protein expression levels of phosphatidylinositol 3-kinase (PI3K), p-PI3K, protein kinase B (Akt), and p-Akt in colonic tissues were analyzed by Western blotting. Molecular docking analysis was performed to evaluate the binding affinity of honokiol with PI3K and Akt. Results Compared with the model group, after treatment with honokiol in UC mice, colonic length was significantly increased, while the colon weight/length ratio, spleen index, and CMDI score were significantly reduced (P < 0.01); histopathological damage was alleviated; expression of TNF-α, IL-6, and IL-1β was significantly decreased, whereas IL-10 expression was significantly upregulated (P < 0.01); expression of Caspase-3, p-PI3K/PI3K, and p-Akt/Akt was significantly downregulated (P < 0.01). Molecular docking results showed that honokiol exhibited strong binding affinity to PI3K and Akt. Conclusion Honokiol may exert a protective effect on UC mice by inhibiting the PI3K/Akt signaling pathway

R965

国家自然科学基金资助项目（81960658）；遵义市科技计划课题基金项目［遵市科合HZ字（2023）460号、（2023）454号］；遵义市科技创新团队建设［遵KCTD（2025）90号］；遵义市科技创新中心（遵市科合CXZX〔2025〕6号）