Lin Peng, Li Baitao, Ye Junli, Shang Fangfang, Zhao Hui, Xie Jing, Yu Xiaoling
Department of Physiology and Pathophysiology, School of Basic Medicine, Qingdao University, Qingdao, Shandong 266021, P.R. China.
Department of Biotechnology, School of Basic Medicine, Qingdao University, Qingdao, Shandong 266021, P.R. China.
Exp Ther Med. 2021 Jun;21(6):548. doi: 10.3892/etm.2021.9980. Epub 2021 Mar 24.
Curcumin is natural polyphenol from rhizomes with several biological properties. Our previous studies demonstrated that curcumin inhibited functional gastric emptying disorders induced by L-arginine, the precursor of nitric oxide (NO), and atropine, an acetylcholine receptor (AChR) blocker. However, the mechanism of action of curcumin remains unclear. In the present study, mouse models of functional gastric emptying disorders induced by L-arginine and atropine were used to examine changes in interstitial cells of Cajal (ICC) and NO- and ACh-mediated regulation of gastrointestinal motility. Curcumin pre-treatment ameliorated the gastric emptying rate in mice treated with L-arginine or atropine (P<0.01). NO content and NO synthase activity significantly increased in the stomachs of L-arginine-treated mice, compared with controls (P<0.01). Acetylcholinesterase activity (P<0.01) and mRNA expression (P<0.01), as well as AChR mRNA levels (P<0.05) significantly decreased following atropine treatment. Moreover, in both models, the levels of c-kit, anoctamin 1 and connexin 43 significantly decreased in the stomach (P<0.01). Conversely, curcumin pre-treatment inhibited the changes induced by L-arginine and atropine (P<0.01 or P<0.05). By affecting the production of exogenous NO, the effects of Ach-AchR and the biomarkers of ICC, curcumin relieves the gastric emptying dysfunction in mice.
姜黄素是一种来自根茎的天然多酚,具有多种生物学特性。我们之前的研究表明,姜黄素可抑制由一氧化氮(NO)的前体L-精氨酸和乙酰胆碱受体(AChR)阻滞剂阿托品诱导的功能性胃排空障碍。然而,姜黄素的作用机制仍不清楚。在本研究中,使用由L-精氨酸和阿托品诱导的功能性胃排空障碍小鼠模型,来检查 Cajal间质细胞(ICC)的变化以及NO和ACh介导的胃肠动力调节。姜黄素预处理改善了用L-精氨酸或阿托品处理的小鼠的胃排空率(P<0.01)。与对照组相比,L-精氨酸处理的小鼠胃中NO含量和NO合酶活性显著增加(P<0.01)。阿托品处理后,乙酰胆碱酯酶活性(P<0.01)和mRNA表达(P<0.01)以及AChR mRNA水平(P<0.05)显著降低。此外,在两种模型中,胃中c-kit、八聚体通道蛋白1和连接蛋白43的水平均显著降低(P<0.01)。相反,姜黄素预处理抑制了由L-精氨酸和阿托品诱导的变化(P<0.01或P<0.05)。通过影响外源性NO的产生、Ach-AChR的作用以及ICC的生物标志物,姜黄素可缓解小鼠的胃排空功能障碍。