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中国医学科学院 北京协和医学院 北京协和医院中医科,北京 100730
Received:28 May 2024,
Published:25 July 2025
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何怡芊,屈岭.黄芪多糖对糖尿病及其慢性并发症的影响及机制研究进展[J].北京中医药,2025,44(7):934-940.
HE Yiqian,QU Ling.Effects and mechanisms of Astragalus polysaccharide in diabetes mellitus and its chronic complications[J]. Beijing Journal of Traditional Chinese Medicine,2025,44(07):934-940.
何怡芊,屈岭.黄芪多糖对糖尿病及其慢性并发症的影响及机制研究进展[J].北京中医药,2025,44(7):934-940. DOI: 10.16025/j.1674-1307.2025.07.026.
HE Yiqian,QU Ling.Effects and mechanisms of Astragalus polysaccharide in diabetes mellitus and its chronic complications[J]. Beijing Journal of Traditional Chinese Medicine,2025,44(07):934-940. DOI: 10.16025/j.1674-1307.2025.07.026.
糖尿病及其慢性并发症是重要的公共卫生问题。近年来研究发现黄芪多糖在防治糖尿病及其慢性并发症方面具有积极作用。黄芪多糖主要从两方面影响糖尿病的进展:一方面,黄芪多糖通过激活磷脂酰肌醇三激酶/蛋白激酶B(PI3K/Akt)信号通路,或抑制微小RNA的表达,从而改善胰岛β细胞的活力和功能,促进胰岛素分泌,抑制血糖升高;另一方面,黄芪多糖通过激活PI3K/Akt信号通路或信号转导及转录激活蛋白(STAT5)促进肝脏和骨骼肌对葡萄糖的吸收、利用与转化,改善胰岛素抵抗。黄芪多糖对糖尿病视网膜病变的作用机制可能是通过影响微小RNA的表达,干预靶蛋白沉默信息调节因子1(SIRT1)、蛋白激酶R样内质网激酶(PERK)和肌醇需求酶1(IRE1)、转录因子6(ATF6)信号通路蛋白表达,或调控Akt-血管内皮生长因子(VEGF)信号通路,影响视网膜新生血管生成,进而保护视网膜色素上皮细胞;黄芪多糖可通过调节肾素-血管紧张素系统(RAS)、改善肾脏病理变化,或作用于腺苷酸活化蛋白激酶(AMPK)/SIRT1等信号通路,减轻肾脏损伤、抗炎等作用机制,抑制糖尿病肾病发生发展;黄芪多糖能够通过多种作用途径改善糖尿病心肌病,主要包括抗氧化应激、减轻内质网应激、促进自噬以及调控骨形态发生蛋白10(BMP10)相关信号等机制,从而保护心肌细胞、抑制心室重构,改善心脏功能和血流动力学;另外,黄芪多糖在糖尿病溃疡、糖尿病肌少症、糖尿病血管内皮病变和糖尿病认知功能障碍的防治中亦发挥积极作用。
Diabetes mellitus and its chronic complications are important public health concerns. Recent studies have shown that
Astragalus
polysaccharide (APS) plays an active role in the prevention and treatment of diabetes mellitus and its chronic complications. APS primarily affects diabetes progression through two mechanisms. First, it improves the viability and function of pancreatic β-cells by activating the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway or inhibiting microRNA expression, thereby promoting insulin secretion and reducing hyperglycemia. Second, APS improves insulin resistance by promoting glucose uptake, utilization, and transformation in the liver and skeletal muscle via activation of the PI3K/Akt or signal transducer and activator of transcription 5 (STAT5) pathways. In diabetic retinopathy, APS may act by regulating microRNA expression and modulating pathways involving silent information regulator 1 (SIRT1), protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1 (IRE1), and activating transcription factor 6 (ATF6), or by regulating the Akt-vascular endothelial growth factor (VEGF) axis, thereby inhibiting retinal neovascularization and protecting retinal pigment epithelial cells. In diabetic nephropathy, APS may alleviate renal injury and inflammation by modulating the renin-
angiotensin system (RAS), improving pathological changes of the kidneys, or activating AMP-activated protein kinase (AMPK)/SIRT1 signaling pathway, thus preventing disease progression. APS also protects against diabetic cardiomyopathy through multiple mechanisms, including antioxidant effects, attenuation of endoplasmic reticulum stress, promotion of autophagy, and regulation of bone morphogenetic protein 10 (BMP10)-related signaling, thereby protecting cardiomyocytes, preventing ventricular remodeling, and improving cardiac function and hemodynamics. In addition, APS demonstrates therapeutic potential in diabetic ulcers, diabetic sarcopenia, vascular endothelial dysfunction, and diabetes-associated cognitive impairment.
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