Icariin is a flavonol glycoside. Icariin inhibits PDE5 and PDE4 activities with IC50 of 432 nM and 73.50 μM, respectively. Icariin also is a PPARα activator[1]. It has exert anti-oxidative, anti-neuroinflammatory, and anti-apoptotic effects[2].
In vitro experiment it shown that treatment of 10 or 20 μM induced 13.1 ± 2.1% and 18.2 ± 1.6% apoptosis in MDA‐MB‐453 cells respectively in comparison with control group. 4T1 cells were treated with 20 μM icariin triggered cell apoptosis[3].
In vivo, rats were injected in 50 mg/kg Icariin significantly reduced paw swelling in carrageenan-injected animals and ameliorated carrageenan-induced paw histopathological alterations. Icariin obviously increased paw enzymatic and non-enzymatic antioxidants and decreased paw lipid peroxidation. Icariin decreased paw levels of inflammatory cytokines and NF-kB[4].
In vivo, rats were administrated with 25 mg/kg and 50 mg/kg icariin improved depression symptoms via regulation of the PI3K-AKT pathway, boosted the expression of the regulatory methylene p85 and catalytic methylene p110 of PI3K, increased the relative expression of p-AKT, and encouraged the expression of the anti-apoptosis factor Bcl-2, thus elevating the ratio of Bcl-2/Bax[5]. In vivo, C57BL/6 J mice were administrated with 50 mg/kg/d icariin effectively attenuated alcohol consumption-induced atrial structural and electrical remodeling[6].
References:
[1] Xin ZC, et al. Effects of icariin on cGMP-specific PDE5 and cAMP-specific PDE4 activities. Asian J Androl. 2003 Mar;5(1):15-8.
[2] Jin J, et al. An outline for the pharmacological effect of icariin in the nervous system. Eur J Pharmacol. 2019 Jan 5;842:20-32.
[3] Song L, et al. Icariin-induced inhibition of SIRT6/NF-κB triggers redox mediated apoptosis and enhances anti-tumor immunity in triple-negative breast cancer. Cancer Sci. 2020 Nov;111(11):4242-4256.
[4] El-Shitany NA, Eid BG. Icariin modulates carrageenan-induced acute inflammation through HO-1/Nrf2 and NF-kB signaling pathways. Biomed Pharmacother. 2019 Dec;120:109567.
[5] Cao LH, et al. PI3K-AKT Signaling Activation and Icariin: The Potential Effects on the Perimenopausal Depression-Like Rat Model. Molecules. 2019 Oct 15;24(20):3700.
[6] Yu LM, et al. Icariin attenuates excessive alcohol consumption-induced susceptibility to atrial fibrillation through SIRT3 signaling. Biochim Biophys Acta Mol Basis Dis. 2022 Oct 1;1868(10):166483.
淫羊藿甙是一种黄酮醇糖苷。淫羊藿甙抑制PDE5和PDE4活性的IC50分别为432 nM和73.50 μM。淫羊藿甙也是PPARα激活剂[1]。它具有抗氧化、抗炎和抗细胞凋亡的作用[2]。
体外实验表明，与对照组相比，10或20 μM淫羊藿甙处理分别诱导MDA‐MB‐453细胞凋亡13.1±2.1%和18.2±1.6%。用20 μM 淫羊藿甙处理4T1细胞，引发细胞凋亡[3]。
在体内，大鼠注射50 mg/kg的淫羊藿甙显著减少了卡拉胶注射动物的爪子肿胀，并改善了卡拉胶诱导的爪子组织病理学改变。淫羊藿甙能明显增加爪酶和非酶抗氧化剂，降低爪脂过氧化。淫羊藿甙降低了爪子炎症细胞因子和NF-kB的水平[4]。在体内，给予25 mg/kg和50 mg/kg的淫羊藿甙通过调节PI3K-AKT通路改善抑郁症状，增强PI3K的调节性亚甲基p85和催化性亚甲基p110的表达，增加p-AKT的相对表达，并促进抗凋亡因子Bcl-2的表达，从而提高Bcl-2/Bax的比例[5]。在体内，C57BL/6 J小鼠给予50 mg/kg/d的淫羊藿甙，有效地减轻了饮酒诱导的心房结构和电重构[6]。