Kaempferol is a flavonoid that acts as an inverse agonist of ERRα and ERRγ and possesses antioxidant, anti-inflammatory and antitumor activities[1-2].
Kaempferol significantly inhibited the activity of HCCC9810 and QBC939 cells in a time- and dose-dependent manner. The IC50 values of Kaempferol-treated cells for 72 h were 58.99 μM and 74.91 μM respectively. Kaempferol inhibits the migration and invasion of HCCC9810 and QBC939 cells in a dose-dependent manner and induces apoptosis[1]. In A2780 OC cells, Kaempferol promoted cell apoptosis (158%), inhibited cell viability (53.17%) and cell proliferation (49.17%). Kaempferol increased the protein levels of GRP78, PERK, ATF6, IRE-1, LC3II, beclin 1 and caspase 4, and activated cytotoxic autophagy[3].
Kaempferol (20 mg/kg) inhibited the growth of mouse tumors in a QBC939 cell xenograft model. In a lung metastasis model simulated by injecting QBC939 cells into nude mice, Kaempferol (20 mg/kg) significantly reduced the number and volume of lung metastatic nodules[1]. Kaempferol can reduce plasma glucose levels and increase insulin levels in diabetic rats. Compared with 50 and 200 mg/kg, 100 mg/kg of Kaempferol showed the greatest hypoglycemic effect. After Kaempferol was administered to diabetic rats, lipid peroxidation products, enzymes, and non-enzyme antioxidants all returned to near normal levels[4].
References:
[1] Youyou Qin, Wu Cui, Xuewei Yang, Baifeng Tong, Kaempferol inhibits the growth and metastasis of cholangiocarcinoma in vitro and in vivo, Acta Biochimica et Biophysica Sinica, Volume 48, Issue 3, March 2016, Pages 238–245.
[2] Wang J, Fang F, Huang Z, et al. Kaempferol is an estrogen-related receptor α and γ inverse agonist[J]. FEBS letters, 2009, 583(4): 643-647.
[3] El-Kott A F, Shati A A, Al-Kahtani M A, et al. Kaempferol Induces Cell Death in A2780 Ovarian Cancer Cells and Increases Their Sensitivity to Cisplatin by Activation of Cytotoxic Endoplasmic Reticulum-Mediated Autophagy and Inhibition of Protein Kinase B[J]. Folia Biologica (00155500), 2020, 66(1).
[4] Al-Numair K S, Chandramohan G, Veeramani C, et al. Ameliorative effect of kaempferol, a flavonoid, on oxidative stress in streptozotocin-induced diabetic rats[J]. Redox Report, 2015, 20(5): 198-209.
Kaempferol是一种黄酮类化合物，可作为ERRα和ERRγ的反向激动剂，具有抗氧化、抗炎和抗肿瘤活性[1-2]。
Kaempferol显著抑制HCCC9810和QBC939细胞的活性，且呈时间和剂量依赖性， Kaempferol处理细胞72 h的IC50值分别为58.99 μM和74.91 μM。Kaempferol以剂量依赖性方式抑制HCCC9810和QBC939细胞的迁移和侵袭，并诱导细胞凋亡[1]。在A2780 OC细胞中，Kaempferol促进了细胞凋亡（158 %），抑制了细胞活力（53.17 %）和细胞增殖（49.17 %）。Kaempferol可增加GRP78、PERK、ATF6、IRE-1、LC3II、beclin 1和caspase 4的蛋白质水平，激活细胞毒性自噬[3]。
Kaempferol（20 mg/kg）可抑制QBC939细胞异种移植模型中小鼠肿瘤的生长。在注射QBC939细胞至裸鼠体内模拟的肺转移模型中，Kaempferol（20 mg/kg）显著减少了肺转移结节数量和体积[1]。Kaempferol可降低糖尿病大鼠的血浆葡萄糖水平，提高胰岛素水平，与50和200mg/kg相比，100mg/kg的Kaempferol显示出最大的降糖作用。给糖尿病大鼠服用Kaempferol后，脂质过氧化产物、酶和非酶抗氧化剂都恢复到接近正常水平[4]。