Astragalin is a natural flavonoid compound with strong antioxidant and anti-inflammatory activities and has shown potential therapeutic applications in various diseases, including cancer and cardiovascular diseases[1]. Astragalin is extracted from plants such as Mongolian milkvetch (Astragalus membranaceus) and sumac (Rhus chinensis)[2]. In cancer research, Astragalin has been reported to inhibit the proliferation of cancer cells and induce apoptosis[3]. Astragalin also protects the cardiovascular system by reducing oxidative stress and inflammation[4].
In vitro, Astragalin (0–100µM) treatment of human colorectal epithelial cells (HCT-116 and HT-29) significantly inhibited cell proliferation. Pre-treatment with Astragalin significantly reduced the mRNA expression levels of tumor necrosis factor-α (TNF-α)-induced interleukin-6 (IL-6), IL-8, and TNF-α. Additionally, Astragalin inhibited the phosphorylation and degradation of IκBα induced by TNF-α and reduced the DNA-binding activity of NF-κB[5]. Astragalin (1–20µM) treatment of human bronchial epithelial cells (BEAS-2B) significantly inhibited the epithelial-mesenchymal transition (EMT) process induced by oxidative stress. Astragalin restored the reduced expression of E-cadherin induced by H₂O₂ and dose-dependently inhibited the expression of vimentin and the formation of autophagosomes[6].
In vivo, Astragalin (10, 20, 40mg/kg) was administered via intraperitoneal injection to APP/PS1 transgenic mice once daily for one month. Astragalin significantly improved cognitive dysfunction in APP/PS1 mice. Astragalin also alleviated neuronal damage in the hippocampus, reduced amyloid-β (Aβ) deposition and the number of senile plaques, and activated autophagy by promoting the expression of autophagy-related proteins (LC3B, Beclin-1, ATG5, ATG12, and LAMP-1). Furthermore, Astragalin inhibited the phosphorylation levels of PI3K/Akt-mTOR signaling pathway-related proteins, thereby exerting neuroprotective effects[7]. Astragalin (5, 10mg/kg/day) was administered orally to streptozotocin (STZ)-induced diabetic mice for 4 weeks. Astragalin significantly improved proteinuria and reduced serum creatinine levels in diabetic mice. Astragalin also alleviated renal pathological damage. Astragalin significantly inhibited the activity of aldose reductase (ALR2) in the kidneys, reduced oxidative stress, improved mitochondrial dysfunction, promoted mitochondrial biogenesis, maintained mitochondrial dynamic balance, and reduced renal cell apoptosis by activating the AMPK-dependent PGC1α pathway[8].
References:
[1] Chen J, Zhong K, Qin S, et al. Astragalin: a food-origin flavonoid with therapeutic effect for multiple diseases. Front Pharmacol. 2023 Oct 18;14:1265960.
[2] Riaz A, Rasul A, Hussain G, et al. Astragalin: A Bioactive Phytochemical with Potential Therapeutic Activities. Adv Pharmacol Sci. 2018 May 2;2018:9794625.
[3] Ruan J, Shi Z, Cao X, et al. Research Progress on Anti-Inflammatory Effects and Related Mechanisms of Astragalin. Int J Mol Sci. 2024 Apr 19;25(8):4476.
[4] Zhang Q, Yan Y. The role of natural flavonoids on neuroinflammation as a therapeutic target for Alzheimer's disease: a narrative review. Neural Regen Res. 2023 Dec;18(12):2582-2591.
[5] Han YM, Koh J, Kim JH, et al. Astragalin Inhibits Nuclear Factor-κB Signaling in Human Colonic Epithelial Cells and Attenuates Experimental Colitis in Mice. Gut Liver. 2021 Jan 15;15(1):100-108.
[6] Cho IH, Choi YJ, Gong JH, et al. Astragalin inhibits autophagy-associated airway epithelial fibrosis. Respir Res. 2015 Apr 21;16(1):51.
[7] Yang CZ, Wang SH, Zhang RH, et al. Neuroprotective effect of astragalin via activating PI3K/Akt-mTOR-mediated autophagy on APP/PS1 mice. Cell Death Discov. 2023 Jan 21;9(1):15.
[8] Sun MY, Ye HJ, Zheng C, et al. Astragalin ameliorates renal injury in diabetic mice by modulating mitochondrial quality control via AMPK-dependent PGC1α pathway. Acta Pharmacol Sin. 2023 Aug;44(8):1676-1686.
Astragalin是一种具有强抗氧化和抗炎活性的天然黄酮类化合物，在多种疾病（包括癌症和心血管疾病）中显示出潜在的治疗应用价值[1]。Astragalin是一种从植物如蒙古黄芪（Astragalus membranaceus）和漆树（Rhus chinensis）中提取的天然黄酮类化合物[2]。在癌症研究中，Astragalin被报道可以抑制癌细胞的增殖并诱导细胞凋亡[3]。Astragalin还通过减少氧化应激和炎症对心血管系统起到保护作用[4]。
在体外，Astragalin（0-100μM）处理人结肠上皮细胞（HCT-116和HT-29），显著抑制了细胞的增殖。Astragalin预处理显著降低了肿瘤坏死因子-α（TNF-α）诱导的白细胞介素-6（IL-6）、白细胞介素-8（IL-8）和TNF-α的mRNA表达水平。此外，Astragalin抑制了TNF-α诱导的IκBα的磷酸化和降解，并降低了NF-κB的DNA结合活性[5]。Astragalin（1-20μM）处理人支气管上皮细胞（BEAS-2B），显著抑制了氧化应激诱导的上皮-间充质转化（EMT）过程。Astragalin恢复了H₂O₂诱导的E-钙黏蛋白（E-cadherin）表达的降低，并剂量依赖性地抑制了波形蛋白（vimentin）的表达，并减少了自噬体的形成[6]。
在体内，Astragalin（10、20、40mg/kg）通过腹腔注射的方式对APP/PS1转基因小鼠进行治疗，每天一次，持续一个月。Astragalin显著改善了APP/PS1小鼠的认知功能障碍，Astragalin减轻了小鼠海马区的神经元损伤，降低了Aβ沉积和老年斑的数量，并通过激活自噬相关蛋白（LC3B、Beclin-1、ATG5、ATG12和LAMP-1）的表达，促进了自噬的启动、自噬体的形成和自噬溶酶体的降解，同时抑制了PI3K/Akt-mTOR信号通路相关蛋白的磷酸化水平，从而发挥了神经保护作用[7]。Astragalin（5、10mg/kg/day）通过口服方式对链脲佐菌素（STZ）诱导的糖尿病小鼠进行治疗，持续4周。Astragalin显著改善了糖尿病小鼠的蛋白尿，降低了血清肌酐水平，减轻了肾脏病理损伤。Astragalin显著抑制了肾脏中醛糖还原酶（ALR2）的活性，降低了氧化应激水平，改善了线粒体功能障碍，促进了线粒体生物合成，维持了线粒体动态平衡，并通过激活AMPK依赖的PGC1α通路减少了肾脏细胞凋亡[8]。