Emodin is a bioactive anthraquinone with anti-tumor, anti-bacterial, and vasorelaxant effects [1]. Emodin inhibits the adhesion of many tumor cells by suppressing lipid raft coalescence and interfering with integrin clustering and focal adhesion complex (FAC) formation [2]. Emodin has been widely used to down-regulate the expression of estrogen receptor α (ERα) and inhibit the proliferation of breast cancer cells[3].
In vitro, Emodin treatment for 72 hours significantly inhibited the proliferation of A549 cells, with an IC50 value of 16.85μg/ml, and caused the cells to shrink in size[4]. Treatment with 60µM Emodin for 48 hours significantly increased the p53 protein level in HepG2/C3A cells, activated the expression of Caspase-3, and induced cell arrest at the G2/M phase[5]. Treatment with 3µM Emodin for 5 days significantly inhibited apoptosis of human umbilical vein endothelial cells (HUVECs) induced by high glucose (22.2mM), reduced CCL5 expression, and prevented the activation of p38 MAPK and ERK1/2 caused by high glucose[6].
In vivo, Emodin treatment via intraperitoneal injection at a dose of 10mg/kg, every other day, for 10 days, inhibited the synovial inflammation and joint destruction in mice with collagen-induced arthritis (CIA), and reduced the production of pro-inflammatory cytokines in joint tissues and serum[7]. Oral administration of Emodin at the 100mg/kg dose twice daily for 35 days significantly improved the metabolic abnormalities in diet-induced obese (DIO) mice, and reduced serum insulin levels and lipid levels[8].
References:
[1] Monisha B A, Kumar N, Tiku A B. Emodin and its role in chronic diseases[J]. Anti-inflammatory nutraceuticals and chronic diseases, 2016: 47-73.
[2] Hsu S C, Chung J G. Anticancer potential of emodin[J]. BioMedicine, 2012, 2(3): 108-116.
[3] Huang P H, Huang C Y, Chen M C, et al. Emodin and aloe‐emodin suppress breast cancer cell proliferation through ERα inhibition[J]. Evidence‐based Complementary and Alternative Medicine, 2013, 2013(1): 376123.
[4] Li W Y, Ng Y F, Zhang H, et al. Emodin elicits cytotoxicity in human lung adenocarcinoma A549 cells through inducing apoptosis[J]. Inflammopharmacology, 2014, 22(2): 127-134.
[5] Shieh D E, Chen Y Y, Yen M H, et al. Emodin-induced apoptosis through p53-dependent pathway in human hepatoma cells[J]. Life sciences, 2004, 74(18): 2279-2290.
[6] Gao Y, Zhang J, Li G, et al. Protection of vascular endothelial cells from high glucose-induced cytotoxicity by emodin[J]. Biochemical Pharmacology, 2015, 94(1): 39-45.
[7] Hwang J K, Noh E M, Moon S J, et al. Emodin suppresses inflammatory responses and joint destruction in collagen-induced arthritic mice[J]. Rheumatology, 2013, 52(9): 1583-1591.
[8] Feng Y, Huang S, Dou W, et al. Emodin, a natural product, selectively inhibits 11β‐hydroxysteroid dehydrogenase type 1 and ameliorates metabolic disorder in diet‐induced obese mice[J]. British Journal of Pharmacology, 2010, 161(1): 113-126.
Emodin是一种具有抗肿瘤、抗菌和血管舒张活性的生物活性蒽醌类化合物[1]。Emodin通过抑制脂筏聚集、干扰整合素簇集和黏着斑复合物(FAC)的形成，从而抑制多种肿瘤细胞的黏附[2]。Emodin已被广泛用于下调雌激素受体α(ERα)的表达并抑制乳腺癌细胞的增殖[3]。
在体外，Emodin处理72小时显著抑制了A549细胞的增殖，IC50值为16.85µg/ml，并导致细胞体积缩小[4]。用60µM的Emodin处理HepG2/C3A细胞48小时，显著提高了p53蛋白水平，激活了Caspase-3的表达，并诱导细胞阻滞在G2/M期[5]。用3µM的Emodin处理人脐静脉内皮细胞(HUVECs) 5天，显著抑制了高糖(22.2mM)诱导的细胞凋亡，降低了CCL5表达，并阻止了高糖引起的p38 MAPK和ERK1/2的激活[6]。
在体内，每隔一天腹腔注射10mg/kg剂量的Emodin，连续10天，抑制了胶原诱导的关节炎(CIA)小鼠的滑膜炎症和关节破坏，并减少了关节组织和血清中促炎细胞因子的产生[7]。每日两次口服100mg/kg剂量的Emodin，连续35天，显著改善了饮食诱导肥胖(DIO)小鼠的代谢异常，并降低了血清胰岛素水平和血脂水平[8]。