Sedanolide, one type of phthalein, is a potent hMAO-B inhibitor with an IC50 value of 0.124±0.033µM [1]. Sedanolide has COX-I and COX-II inhibitory activities and topoisomerase-I and topoisomerase-II inhibitory activities[2]. Sedanolide has been widely used in a variety of cancer cell models to inhibit cell growth and has inhibitory effects on a variety of bacteria and fungi[3].
In vitro, Sedanolide treatment at 500μM for 24 hours induced autophagy in J5 cells, which inhibited the PI3K/Akt/mTOR pathway[4]. Treatment with 500μM Sedanolide for 24h resulted in a significant increase in DNA strand breaks in HepG2 cells[5]. Treatment with 100μM Sedanolide for 24h protected luciferase-expressing HepG2 cells from H2O2-induced cell death and reduced intracellular ROS levels[6].
In vivo, Sedanolide treatment via daily administration at a dose of 20mg/kg/day for 14 consecutive days protected mice from dextran sodium sulfate (DSS)-induced colitis, alleviated intestinal inflammation, and enhanced intestinal barrier function[7]. Oral administration of Sedanolide (10mg/kg/day) for 14 consecutive days can activate the Nrf2 pathway and alleviate liver damage in mice treated with Acetaminophen (APAP)[8].
References:
[1] Fan Y, Wang J, Jian J, et al. High-throughput discovery of highly selective reversible hMAO-B inhibitors based on at-line nanofractionation[J]. Acta Pharmaceutica Sinica B, 2024, 14(4): 1772-1786.
[2] Momin R A, Nair M G. Antioxidant, cyclooxygenase and topoisomerase inhibitory compounds from Apium graveolens Linn. seeds[J]. Phytomedicine, 2002, 9(4): 312-318.
[3] Xie Q, Zhang X, Zhao S, et al. Sedanolide: A review on its chemical compounds, mechanisms and functions[J]. Fitoterapia, 2025: 106732.
[4] Hsieh S L, Chen C T, Wang J J, et al. Sedanolide induces autophagy through the PI3K, p53 and NF-κB signaling pathways in human liver cancer cells[J]. International journal of oncology, 2015, 47(6): 2240-2246.
[5] Woods J A, Jewell C, O'Brien N M. Sedanolide, a natural phthalide from celery seed oil: effect on hydrogen peroxide and tert-butyl hydroperoxide-induced toxicity in HepG2 and CaCo-2 human cell lines[J]. In Vitro & Molecular Toxicology: A Journal of Basic and Applied Research, 2001, 14(3): 233-240.
[6] Tabei Y, Abe H, Suzuki S, et al. Sedanolide activates KEAP1–NRF2 pathway and ameliorates hydrogen peroxide-induced apoptotic cell death[J]. International journal of molecular sciences, 2023, 24(22): 16532.
[7] Li S, Zhuge A, Chen H, et al. Sedanolide alleviates DSS-induced colitis by modulating the intestinal FXR-SMPD3 pathway in mice[J]. Journal of Advanced Research, 2025, 69: 413-426.
[8] Li S, Zhuge A, Xia J, et al. Bifidobacterium longum R0175 protects mice against APAP-induced liver injury by modulating the Nrf2 pathway[J]. Free Radical Biology and Medicine, 2023, 203: 11-23.
Sedanolide是一种苯酞类化合物，作为高效的hMAO-B抑制剂，IC50值为0.124±0.033µM[1]。Sedanolide兼具对COX-I和COX-II与拓扑异构酶-I和拓扑异构酶-II的抑制活性[2]。Sedanolide已在多种癌细胞模型中广泛应用于抑制细胞生长，并对多种细菌和真菌表现出抑制作用[3]。
在体外，使用500μM的Sedanolide处理J5细胞24小时可通过抑制PI3K/Akt/mTOR通路诱导细胞自噬[4]。500μM的Sedanolide处理HepG2细胞24小时可显著引起DNA链断裂[5]。100μM的Sedanolide处理表达荧光素酶的HepG2细胞24小时，能保护细胞免受过氧化氢诱导的死亡，并降低细胞内活性氧水平[6]。
在体内，连续14天每日口服20mg/kg/day剂量的Sedanolide，可保护小鼠免受葡聚糖硫酸钠(DSS)诱导的结肠炎损伤，减轻肠道炎症并增强肠道屏障功能[7]。连续14天每日口服10mg/kg/day剂量的Sedanolide，能激活Nrf2通路并缓解对乙酰氨基酚(APAP)引起的小鼠肝损伤[8]。