Vicenin 2 is an orally active angiotensin-converting enzyme (ACE) inhibitor with the IC50 value of 43.83 ± 3.01μM[1]. Vicenin 2 has anti-inflammatory and antioxidant properties which make it potential applications in various fields, including skin health and cancer therapy.
In vitro, Vicenin 2 (6.25–400μM) incubated human dermal fibroblast (HDF) cell for 24h. Vicenin 2 treatment on HDF cells enhanced cell proliferation in a dose-dependent up to 50μM, but the higher concentrations inhibited proliferation. Low concentrations of Vicenin 2 (12.5 and 25μM) have significantly induced the cell migration and wound closure, while higher concentrations (50 and 100µM) reduced these effects. In addition, treatment with 100μM of Vicenin 2 on HDF significantly increased the expression of inflammatory cytokines and higher expression for inflammatory mediators (NF-κB, iNOS, and COX-2) and healing growth factors (VEGF and TGF-β) proteins[2]. Vicenin 2 (40μM) incubation for 24 hours can restore the antioxidant defense of human gastric epithelial cells (GES-1) by modulating key signaling pathways (PI3K/AKT and MAPK) and upregulating Nrf2 expression, effectively protecting them from cytotoxicity, oxidative stress, DNA damage, and inflammation induced by Helicobacter pylori. These findings suggest that Vicenin 2 could serve as a potential therapeutic agent for preventing H. pylori-induced gastric carcinogenesis[3]. NCI-H23 cells were treated with 10–100µM of Vicenin 2 for 24h. There was a gradual reduction in the percent surviving cells from 60µM to 100µM. NCI-H23 cells treated with radiation exposure with and without 80µM Vicenin 2 suggested that there was greater reduction in percent cell survival with Vicenin 2 treatment. Vicenin 2 showed a potent radiosensitizing property while also showing chemotherapeutic property against Non-small cell lung cancer (NSCLC) cell line NCI-H23[4].
In vivo,Vicenin 2 (50mg/kg/day) administered orally via oral gavage tube into dextran sulfate sodium-induced colitis mice model for 7 days exerted therapeutic effects by the inhibition of pro-inflammatory mediators (iNOS and COX-2) and suppression of specific inflammatory markers expression[5]. In a study on ovariectomy (OVX)-induced osteoporosis rat models, Vicenin 2 orally administered at doses of 5mg/kg/day or 10mg/kg/day for 12 consecutive weeks significantly improved body mass, uterus index, lipid profiles, and inflammatory markers. Vicenin 2 also reduced bone turnover markers and increased serum calcium levels in the OVX rats. These results suggested that Vicenin 2 could be an excellent candidate to treat and manage bone related disease or disorders[6]. The administration of Vicenin 2 (23.8µg/mouse) into LPS-induced lethal endotoxemia model given twice at 12 and 50 hours post-LPS injection, significantly increased survival rates, reduced endothelial cell protein C receptor shedding, decreased pro-inflammatory cytokine expression, protected vascular barrier integrity, and inhibited leukocyte migration. These findings suggest that Vicenin 2 could serve as a potential therapeutic agent for treating severe vascular inflammatory diseases [7].
References:
[1] Zhang YQ, et al. Bioassay-guided preparative separation of angiotensin-converting enzyme inhibitory C-flavone glycosides from Desmodium styracifolium by recycling complexation high-speed counter-current chromatography. J Pharm Biomed Anal. 2015 Jan;102:276-81.
[2] Tan W S, Arulselvan P, Ng S F, et al. Healing Effect of Vicenin-2 (Vicenin-2) on Human Dermal Fibroblast (HDF) and Development Vicenin-2 Hydrocolloid Film Based on Alginate as Potential Wound Dressing. Biomed Res Int. 2020 Apr 23:2020:4730858.
[3] Zhang Y F, Sun J, Dong Y, et al. Vicenin-2 inhibits the Helicobacterium pylori infection associated gastric carcinogenic events through modulation of PI3K/AKT and Nrf2 signaling in GES-1 cells. J Biochem Mol Toxicol. 2021 Mar;35(3):e22680.
[4] Baruah T J, Sharan R N, Kma L. Vicenin-2: a potential radiosensitizer of non-small cell lung cancer cells. Mol Biol Rep. 2018 Oct;45(5):1219-1225.
[5] Yin Y T, Ye L, Niu Z B, Fang W H.Anti-inflammatory effects of Vicenin-2 on dextran sulfate sodium-induced colitis in mice. Drug Dev Res. 2019 Aug;80(5):546-555.
[6] Zhang Z P, Zhao Q P, Liu T J,et al. Effect of Vicenin-2 on ovariectomy-induced osteoporosis in rats. Biomed Pharmacother. 2020 Sep:129:110474.
[7] Kang H J, Ku S K, Jung B K, BaeJ S. Anti-inflammatory effects of vicenin-2 and scolymoside in vitro and in vivo. Inflamm Res. 2015 Dec;64(12):1005-21.
Vicenin 2是一种具有口服活性的血管紧张素转换酶（ACE）抑制剂，IC50值为43.83±3.01μM[1]。Vicenin 2具有抗炎和抗氧化的特性，这使得它在包括皮肤健康和癌症治疗在内的各个领域具有潜在的应用前景。
在体外实验中，Vicenin 2（6.25–400μM）孵育人皮肤成纤维细胞（HDF）24小时。Vicenin 2对HDF细胞的处理在浓度不超过 50μM时能增强细胞增殖，但更高浓度则会抑制增殖。低浓度的Vicenin 2（12.5和25μM）显著诱导细胞迁移和伤口闭合，而更高浓度（50和100μM）则会降低这种效果。此外，用100μM的Vicenin 2处理HDF显著增加了炎症细胞因子的表达，以及炎症介质（NF-κB、iNOS和COX-2）和愈合生长因子（VEGF和TGF-β）蛋白的高表达[2]。Vicenin 2（40μM）孵育 24小时可通过调节关键信号通路（PI3K/AKT和MAPK）并上调Nrf2表达恢复细胞的抗氧化防御，有效保护人胃上皮细胞（GES-1）免受幽门螺杆菌诱导的细胞毒性、氧化应激、DNA损伤和炎症。这表明Vicenin 2可能成为预防幽门螺杆菌诱导的胃癌发生的潜在治疗药物[3]。非小细胞肺癌细胞NCI-H23用10-100μM的Vicenin 2处理24小时，从60μM到100μM，存活细胞的百分比逐渐降低。用或不用80μM Vicenin 2处理经辐射照射的NCI-H23细胞24h后，结果表明Vicenin 2 处理使细胞存活率的降低更显著。Vicenin 2显示出强大的放射增敏特性，同时对非小细胞肺癌细胞系NCI-H23也表现出化疗特性[4]。
在体内实验中，通过口服灌胃管向葡聚糖硫酸钠诱导的结肠炎小鼠模型中每天给予50mg/kg的Vicenin 2，持续7天，Vicenin 2通过抑制促炎介质（诱导型一氧化氮合酶和环氧化酶-2）以及抑制特定炎症标志物的表达，发挥治疗作用[5]。在一项卵巢切除术（OVX）所致骨质疏松大鼠模型的研究中，连续12周口服5mg/kg/day或10mg/kg/day的Vicenin 2可显著改善大鼠体重、子宫指数、脂质分布和炎症指标。Vicenin 2还能降低OVX大鼠的骨转换标志物，提高血清钙水平。这些结果表明，Vicenin 2可能是治疗和管理骨相关疾病或紊乱的优秀候选者[6]。在脂多糖诱导的致死性内毒素血症模型中给予Vicenin 2（每只小鼠23.8μg）治疗，在脂多糖注射后12小时和50小时各给药一次，显著提高了小鼠存活率，减少了内皮细胞蛋白C受体脱落，降低了促炎细胞因子的表达，保护了血管屏障的完整性，并抑制了白细胞迁移，说明Vicenin 2可能是治疗严重血管炎症疾病的潜在治疗药物[7]。