Tanshinone IIA is a major tanshinone isolated from Salvia divinorum. Commonly used in cardiovascular disease and cancer research.
Tanshinone IIA (0.125-4μM; 24h) led to a increase in the percentage of apoptotic HL-60 cells ; the percentage of apoptotic cells increased from 11.4% in the DMSO group to 53% in 2.0μM Tanshinone IIA-treated group[1]. Tanshinone IIA (15, 30, and 60μg/mL; 4h ) can reduce hydrogen peroxide (H2O2)-induced human umbilical vein endothelial cell line (ECV-304) cell damage by increasing superoxide dismutase (SOD) activity and inhibiting cluster of differentiation 40(CD40) inflammatory pathway[2]. Tanshinone IIA (5, 10, and 20μg/μL; 24h) inhibited H2O2-induced reactive oxygen species(ROS) rise and apoptosis in EA. hy926 cells[3].
Tanshinone IIA (20mg/kg/day; po; 16weeks) inhibited the production of IL-1β and IL-18 in aortic tissue and serum of ApoE−/− mice fed a high cholesterol diet (HCD) [4]. Tanshinone IIA (60mg/kg/day; po; 4weeks) inhibited the progression of AS in P. Gingivalis-induced ApoE−/− mice by down-regulating NOX2, NOX4, and NF-κB[5]. Tanshinone IIA (30mg/kg; po; 8weeks) can reduce the expression of MMP-2, MMP-3, MMP-9 and inflammatory factors by inhibiting RAGE/MAPK signaling pathway, thus increasing the stability of atherosclerotic plaques[6].
References:
[1]. Nie ZY, Zhao MH, Cheng BQ, Pan RF, Wang TR, Qin Y, Zhang XJ. Tanshinone IIA regulates human AML cell proliferation, cell cycle, and apoptosis through miR-497-5p/AKT3 axis. Cancer Cell Int. 2020 Aug 7;20:379.
[2]. Lin R, Wang WR, Liu JT, Yang GD, Han CJ. Protective effect of tanshinone IIA on human umbilical vein endothelial cell injured by hydrogen peroxide and its mechanism. J Ethnopharmacol. 2006 Nov 24;108(2):217-22.
[3]. Jia LQ, Yang GL, Ren L, Chen WN, Feng JY, Cao Y, Zhang L, Li XT, Lei P. Tanshinone IIA reduces apoptosis induced by hydrogen peroxide in the human endothelium-derived EA.hy926 cells. J Ethnopharmacol. 2012 Aug 30;143(1):100-8.
[4].Wen J, Chang Y, Huo S, Li W, Huang H, Gao Y, Lin H, Zhang J, Zhang Y, Zuo Y, Cao X, Zhong F. Tanshinone IIA attenuates atherosclerosis via inhibiting NLRP3 inflammasome activation. Aging (Albany NY). 2020 Nov 16;13(1):910-932.
[5].Xuan Y, Yu C, Ni K, Congcong L, Lixin Q, Qingxian L. Protective effects of tanshinone IIA on Porphyromonas gingivalis-induced atherosclerosis via the downregulation of the NOX2/NOX4-ROS mediation of NF-κB signaling pathway. Microbes Infect. 2023 Nov-Dec;25(8):105177.
[6].Zhao D, Tong L, Zhang L, Li H, Wan Y, Zhang T. Tanshinone II A stabilizes vulnerable plaques by suppressing RAGE signaling and NF-κB activation in apolipoprotein-E-deficient mice. Mol Med Rep. 2016 Dec;14(6):4983-4990.
Tanshinone IIA 是一种从丹参中分离出来的主要丹参酮，常用于心血管疾病和癌症的研究。
Tanshinone IIA（0.125-4μM；24h）可增加 HL-60 细胞凋亡的百分比；凋亡细胞的百分比从二甲基亚砜组的 11.4% 增加到 2.0 μM 丹参酮 IIA 处理组的 53%[1]。Tanshinone IIA（15、30 和 60μg/mL；24h）可通过增加超氧化物歧化酶（SOD）活性和抑制分化簇 40（CD40）炎症通路，减轻过氧化氢（H2O2）诱导的人脐静脉内皮细胞系（ECV-304）细胞损伤[2]。Tanshinone IIA（5、10 和 20μg/μL，24h）能抑制 H2O2 诱导的活性氧（ROS）上升和 EA. hy926 细胞的凋亡[3]。
Tanshinone IIA（20mg/kg/day；po；16weeks）可抑制高胆固醇饮食（HCD）载脂蛋白E-/-小鼠主动脉组织和血清中 IL-1β 和 IL-18 的产生[4]。Tanshinone IIA（60mg/kg/day；po；4weeks）通过下调 NOX2、NOX4 和 NF-κB 抑制牙龈脓肿诱导的载脂蛋白E-/-小鼠强直性脊柱炎的进展[5]。Tanshinone IIA（30mg/kg；po；8weeks）可通过抑制 RAGE/MAPK 信号通路，减少 MMP-2、MMP-3、MMP-9 和炎症因子的表达，从而增加动脉粥样硬化斑块的稳定性[6]。