Dihydromyricetin is a natural flavanonol isolated from A. grossedentata and H. dulcis that has antioxidant, antiproliferative, anti-apoptotic, and anti-alcohol intoxication properties[1].
Dihydromyricetin (5, 10, 15; 20; 25; 30μM; 48h) pre-treated MG63 cells for 48 hours, preventing hydrogen peroxide-induced reduction in cell viability. 30μM of Dihydromyricetin during incubation fully blocked the decrease in cell viability caused by 100μM hydrogen peroxide[2]. Dihydromyricetin (12.5, 25, 50μM; 24h) increased the p-STAT3-dependent autophagy by generating ROS-signaling pathways in head and neck squamous cell carcinoma. and inhibiting autophagy could enhance Dihydromyricetin-induced apoptosis in head and neck squamous cell carcinoma[3].
Dihydromyricetin (150mg/kg; po; 4d) showed a strong anti-inflammatory effect on CCl4-induced liver injury in mice, Dihydromyricetin could significantly decrease serum ALT, AST, IL-1β, IL-6 and TNF-α and increase serum albumin, SOD and liver SOD after CCl4 treatment[4].Dihydromyricetin (10mg/kg; ip; 27d) treatment significantly reduced the total number of inflammatory cells in sputum including eosinophils, neutrophils, lymphocytes, and macrophages, as well as the levels of IL-4, IL-5, and IL-13 in BAL fluids, and the secretion of OVA-specific IgE and IgG1 in serum in mice with allergic asthma[5].
[1]. Liu D, Mao Y, Ding L, et al. Dihydromyricetin: A review on identification and quantification methods, biological activities, chemical stability, metabolism and approaches to enhance its bioavailability[J]. Trends in Food Science & Technology, 2019, 91: 586-597.
[2]. Wang Y, Wang W, Qiu E. Protection of oxidative stress induced apoptosis in osteosarcoma cells by Dihydromyricetin through down-regulation of caspase activation and up-regulation of BcL-2[J]. Saudi Journal of Biological Sciences, 2017, 24(4): 837-842.Xu P, Zhang M, Wang X, et al. Antioxidative effect of Quetiapine on acute ultraviolet-B-induced skin and HaCaT cell damage[J]. International Journal of Molecular Sciences, 2018, 19(4): 953.
[3].Fan T F, Wu T F, Bu L L, et al. Dihydromyricetin promotes autophagy and apoptosis through ROS-STAT3 signaling in head and neck squamous cell carcinoma[J]. Oncotarget, 2016, 7(37): 59691.
[4]. Xie J, Liu J, Chen T M, et al. Dihydromyricetin alleviates carbon tetrachloride-induced acute liver injury via JNK-dependent mechanism in mice[J]. World Journal of Gastroenterology: WJG, 2015, 21(18): 5473.
[5].Xu B, Huang S, Wang C, et al. Anti‑inflammatory effects of Dihydromyricetin in a mouse model of asthma[J]. Molecular Medicine Reports, 2017, 15(6): 3674-3680.
Dihydromyricetin是从 A. grossedentata 和 H. dulcis 中分离出来的天然黄烷醇，具有抗氧化、抗增殖、抗凋亡和抗酒精中毒特性[1]。
Dihydromyricetin（5、10、15、20、25、30μM；48h）预处理 MG63 细胞 48 小时，可防止过氧化氢引起的细胞活力降低。孵育期间30μM Dihydromyricetin完全阻断了100μM过氧化氢引起的细胞活力下降[2]。Dihydromyricetin（12.5、25、50μM；24h）通过在头颈部鳞状细胞癌中产生 ROS信号通路来增加p-STAT3依赖性自噬，抑制自噬可增强Dihydromyricetin诱导的头颈部鳞状细胞癌细胞凋亡[3]。
Dihydromyricetin（150mg/kg；po；4d）对CCl4诱导的小鼠肝损伤有较强的抗炎作用，CCl4处理后，Dihydromyricetin可显著降低血清ALT、AST、IL-1β、IL-6和TNF-α，升高血清白蛋白、SOD和肝脏SOD[4]。Dihydromyricetin（10mg/kg；ip；27d）治疗可显著降低哮喘小鼠痰液中嗜酸性粒细胞、中性粒细胞、淋巴细胞和巨噬细胞等炎性细胞总数，降低BAL液中IL-4、IL-5和IL-13的水平，减少血清中OVA特异性IgE和IgG1的分泌[5]。