Medical Research Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu 213003, P.R. China.
Department of Gastrointestinal Surgery, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu 213003, P.R. China.
Mol Med Rep. 2018 Oct;18(4):3691-3698. doi: 10.3892/mmr.2018.9378. Epub 2018 Aug 10.
Sinomenine (SIN), a pure alkaloid isolated from Sinomenium acutum, has been widely used in arthritis for its anti‑inflammatory effect, but little is known about the effect of SIN on human ulcerative colitis (UC). In the present study, the effect and mechanism of SIN was examined in a dextran sulfate sodium (DSS)‑induced murine colitis model, which mimics human UC. Oral administration of SIN significantly suppressed the elevated disease activity index and ameliorated colonic histological damage in a DSS‑induced colitis model. Tumor necrosis factor‑α, interleukin‑6 and inducible nitric oxide synthase levels were also reduced as detected by reverse transcription‑quantitative polymerase chain reaction. In addition, SIN reversed the decreased colon length and colonic superoxide dismutase activity. Furthermore, western blot analysis revealed that nuclear factor‑erythroid 2‑related factor 2 (Nrf2) and its downstream genes, heme oxygenase‑1 and NADP(H) quinone oxidoreductase 1 (NQO‑1), were markedly activated by SIN. The current results indicated that SIN alleviated DSS‑induced colitis in mice, which may be due to its antioxidant properties and was at least in part dependent on the Nrf2/NQO‑1 signaling pathway. Therefore, SIN may have potential applications as a protective drug for patients with UC.
青藤碱（SIN）是从青风藤中分离得到的一种纯生物碱，因其具有抗炎作用而被广泛用于关节炎，但关于 SIN 对人类溃疡性结肠炎（UC）的影响知之甚少。在本研究中，在葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎模型中研究了 SIN 的作用及其机制，该模型模拟了人类 UC。SIN 口服给药可显著抑制 DSS 诱导的结肠炎模型中疾病活动指数的升高，并改善结肠组织学损伤。通过逆转录定量聚合酶链反应检测到肿瘤坏死因子-α、白细胞介素-6 和诱导型一氧化氮合酶水平也降低。此外，SIN 还逆转了结肠长度的缩短和结肠超氧化物歧化酶活性的降低。此外，Western blot 分析表明，核因子-红细胞 2 相关因子 2（Nrf2）及其下游基因血红素加氧酶-1 和 NADP（H）醌氧化还原酶 1（NQO-1）被 SIN 显著激活。目前的结果表明，SIN 缓解了 DSS 诱导的小鼠结肠炎，这可能与其抗氧化特性有关，至少部分依赖于 Nrf2/NQO-1 信号通路。因此，SIN 可能有作为 UC 患者保护药物的应用潜力。
