Li Wan-Ying, Liu Jun-Yang, Wang Zi-Xian, Wang Ke-Ying, Huang Chun-Xiang, He Wen, Song Jia-Le
Department of Nutrition and Food Hygiene, School of Public Health, Guilin Medical University, Guilin 541100, Guangxi, China.
Department of Clinical Nutrition, Liuzhou People's Hospital, Liuzhou 545006, Guangxi, China.
ACS Omega. 2023 Dec 26;9(1):1230-1241. doi: 10.1021/acsomega.3c07474. eCollection 2024 Jan 9.
Ulcerative colitis (UC) is a chronic gastrointestinal disease that results from repeated inflammation and serious complications. Sinapic acid (SA) is a hydroxycinnamic acid present in a variety of plants that has antioxidant, anti-inflammatory, anticancer, and other protective effects. This study investigated the antifibrotic effect of SA on chronic colitis induced by dextran sulfate sodium salt (DSS) in mice. We observed that SA could significantly reduce clinical symptoms (such as improved body weight loss, increased colon length, and decreased disease activity index score) and pathological changes in mice with chronic colitis. SA supplementation has been demonstrated to repair intestinal mucosal barrier function and maintain epithelial homeostasis by inhibiting activation of the NLRP3 inflammasome and decreasing the expression of IL-6, TNF-α, IL-17A, IL-18, and IL-1β. Furthermore, SA could induce the expression of antioxidant enzymes (, , , ) by activating the Nrf2/keap1 pathway, thus improving antioxidant capacity. Additionally, SA could increase the protein expression of downstream LC3-II/LC3-I and Beclin1 and induce autophagy by regulating the AMPK-Akt/mTOR signaling pathway, thereby reducing the production of intestinal fibrosis-associated proteins Collagen-I and α-SMA. These findings suggest that SA can enhance intestinal antioxidant enzymes, reduce oxidative stress, expedite intestinal epithelial repair, and promote autophagy, thereby ameliorating DSS-induced colitis and intestinal fibrosis.
溃疡性结肠炎(UC)是一种由反复炎症和严重并发症引起的慢性胃肠疾病。芥子酸(SA)是一种存在于多种植物中的羟基肉桂酸,具有抗氧化、抗炎、抗癌和其他保护作用。本研究调查了SA对葡聚糖硫酸钠(DSS)诱导的小鼠慢性结肠炎的抗纤维化作用。我们观察到SA可显著减轻慢性结肠炎小鼠的临床症状(如改善体重减轻、增加结肠长度和降低疾病活动指数评分)及病理变化。已证明补充SA可通过抑制NLRP3炎性小体的激活和降低IL-6、TNF-α、IL-17A、IL-18和IL-1β的表达来修复肠黏膜屏障功能并维持上皮稳态。此外,SA可通过激活Nrf2/keap1途径诱导抗氧化酶(、、、)的表达,从而提高抗氧化能力。此外,SA可增加下游LC3-II/LC3-I和Beclin1的蛋白表达,并通过调节AMPK-Akt/mTOR信号通路诱导自噬,从而减少肠道纤维化相关蛋白I型胶原蛋白和α-平滑肌肌动蛋白的产生。这些发现表明,SA可增强肠道抗氧化酶、减轻氧化应激、加速肠上皮修复并促进自噬,从而改善DSS诱导的结肠炎和肠道纤维化。
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