Icariin is a flavonol glycoside. Icariin inhibits PDE5 and PDE4 activities with IC₅₀s of 432 nM and 73.50 μM, respectively. Icariin also is a PPARα activator.

Icariin is a cGMP-specific PDE5 inhibitor. The inhibitory effects of Icariin on PDE5 and PDE4 activities are investigated by the two-step radioisotope procedure with ³H-cGMP/ ³H-cAMP. The potency of selectivity of Icariin on PDE5 (PDE4/PDE5 of IC₅₀) is 167.67 times^[1]. Cell viability is measured in the present study to evaluate whether Icariin protect endothelial HUVECs from injuries induced by oxidized low-density lipoprotein (ox-LDL). The exposure of the cells to ox-LDL for 24 h significantly decreases the cell viability compared with control group (P<0.05). However, Icariin can inhibit cell injury induced by ox-LDL in a concentration-dependent manner, and has significant difference (P<0.05) compared with ox-LDL-simulated group^[3].
Icariin protects BMSCs against OGD-induced apoptosis by inhibiting ERs-mediated (ER Stress) autophagy via MAPK signaling pathway^[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Icariin is a PPARα activator, induces Cyp4a10 and Cyp4a14, and regulates the mRNA levels of lipid metabolism enzymes and proteins, including fatty acid binding protein, fatty acid oxidation in mitochondria and in peroxisome. Icariin is effective in the treatment of hyperlipidemia. To understand the effect of Icariin on lipid metabolism, effects of Icariin on PPARα and its target genes are investigated. Mice are treated orally with Icariin at doses of 0, 100, 200, and 400 mg/kg, or Clofibrate (500 mg/kg) for five days. Liver total RNA is isolated and the expressions of PPARα and lipid metabolism genes are examined. PPARα and its marker genes Cyp4a10 and Cyp4a14 are induced 2-4 fold by Icariin, and 4-8 fold by Clofibrate. The fatty acid (FA) binding and co-activator proteins Fabp1, Fabp4 and Acsl1 are increased 2-fold. The mRNAs of mitochondrial FA β-oxidation enzymes (Cpt1a, Acat1, Acad1 and Hmgcs2) are increased 2-3 fold. The mRNAs of proximal β-oxidation enzymes (Acox1, Ech1, and Ehhadh) are also increased by Icariin and Clofibrate. The expression of mRNAs for sterol regulatory element-binding factor-1 (Srebf1) and FA synthetase (Fasn) are unaltered by Icariin. The lipid lysis genes Lipe and Pnpla2 are increased by Icariin and Clofibrate^[2]. Adult rats are treated orally with Icariin at doses of 0 (control), 50, 100, or 200 mg/kg body weight for 35 consecutive days. The results show that Icariin has virtually no effect on the body weight or organ coefficients of the testes or epididymides. However, 100 mg/kg Icariin significantly increases epididymal sperm counts. In addition, 50 and 100 mg/kg Icariin significantly increase testosterone levels. Furthermore, 100 mg/kg Icariin treatment also affects follicle stimulating hormone receptor (FSHR) and claudin-11 mRNA expression in Sertoli cells. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels are measured in the testes; 50 and 100 mg/kg Icariin treatment improve antioxidative capacity, while 200 mg/kg Icariin treatment upregulates oxidative stress^[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

676.66

C₃₃H₄₀O₁₅

489-32-7

淫羊藿甙；淫羊藿甙

Room temperature in continental US; may vary elsewhere.

DMSO : 125 mg/mL (184.73 mM; Need ultrasonic)

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂：;10% DMSO ;; 90% corn oil

  Solubility: ≥ 2.5 mg/mL (3.69 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (3.69 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• 2.

  请依序添加每种溶剂：;10% DMSO ;; 40% PEG300 ;; 5% Tween-80 ;; 45% saline

  Solubility: ≥ 2.08 mg/mL (3.07 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (3.07 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 3.

  请依序添加每种溶剂：;10% DMSO ;; 90% (20% SBE-β-CD in saline)

  Solubility: 2.08 mg/mL (3.07 mM); Suspended solution; Need ultrasonic

  此方案可获得 2.08 mg/mL (3.07 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明

• [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]. Lu YF, et al. Icariin is a PPARα activator inducing lipid metabolic gene expression in mice. Molecules. 2014 Nov 6;19(11):18179-91.

  [3]. Hu Y, et al. Effects and mechanisms of icariin on atherosclerosis. Int J Clin Exp Med. 2015 Mar 15;8(3):3585-9.

  [4]. Chen M, et al. Effects of icariin on reproductive functions in male rats. Molecules. 2014 Jul 3;19(7):9502-14.

  [5]. Liu D, et al. Icariin protects rabbit BMSCs against OGD-induced apoptosis by inhibiting ERs-mediated autophagy via MAPK signaling pathway. Life Sci. 2020 Apr 26:117730.

Human umbilical vein endothelial cells (HUVECs) in the logarithmic growth phase are seeded into 96-well plates at a density of 1×10⁴ cells per well, then incubated for 24 hours at 37°C, 5% CO₂. After pretreatment with indicated concentration of Icariin (0, 10, 20, 40 μM) for 24 hours, the cells are incubated with or without ox-LDL (100 μg/mL) for next 24 hours. After suction of the liquid in the wells, MTT solution is added to yield a final concentration of 0.5 mg/mL, and incubation is continued for 4 h at 37°C, 5% CO₂. MTT solution is removed gently and 150 μL of DMSO is added to each well for 15 min incubation. The absorbance of each sample is measrured on a microplate reader at 490 nm as cell viability^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Mice^[2]
Adult 8-week old male C57BL/6 mice are acclimated for 1-week in a temperature- and humidity-controlled facility with a standard 12-h light schedule. Mice have free access to SPF-grade rodent chow and purified drinking water. Mice are treated with Icariin (100, 200, and 400 mg/kg) for 5 days. Clofibrate (CLO, 500 mg/kg, po for 5 days) is used as a positive control, for negative controls, mice are given 2% CMC (10 mL/kg). 24 h after the last dose, livers are collected for analysis.
Rats^[4]
Forty adult male SD rats weighing 200-290 g (12-16 weeks old) are randomly assigned to groups (n=10 per group) according to their body weight. The rats receive daily intragastric administration of Icariin at 0 (control), 50, 100, or 200 mg/kg per day for 35 consecutive days. The animals are weighed weekly, and the treatments are adjusted accordingly. At the end of the Icariin treatment period, all rats are sacrificed; blood samples are subsequently collected for further analyses of testosterone levels.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

• [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]. Lu YF, et al. Icariin is a PPARα activator inducing lipid metabolic gene expression in mice. Molecules. 2014 Nov 6;19(11):18179-91.

  [3]. Hu Y, et al. Effects and mechanisms of icariin on atherosclerosis. Int J Clin Exp Med. 2015 Mar 15;8(3):3585-9.

  [4]. Chen M, et al. Effects of icariin on reproductive functions in male rats. Molecules. 2014 Jul 3;19(7):9502-14.

  [5]. Liu D, et al. Icariin protects rabbit BMSCs against OGD-induced apoptosis by inhibiting ERs-mediated autophagy via MAPK signaling pathway. Life Sci. 2020 Apr 26:117730.