黄精多糖的生物学活性及其在相关疾病防治中的作用

管佩瑶; 李子业; 王倩; 丁涵; 陈立章; 秦虹

doi:10.11817/j.issn.1672-7347.2025.250247

中南大学学报（医学版） ›› 2025, Vol. 50 ›› Issue (9) : 1664 -1673. DOI: 10.11817/j.issn.1672-7347.2025.250247

综述

黄精多糖的生物学活性及其在相关疾病防治中的作用

管佩瑶 ¹ ,
李子业 ¹ ,
王倩 ² ,
丁涵 ¹ ,
陈立章 ¹ ,
秦虹 ¹

作者信息 +

Biological activities of Polygonatum polysaccharides and their roles in the prevention and treatment of related diseases

Peiyao GUAN ¹ ,
Ziye LI ¹ ,
Qian WANG ² ,
Han DING ¹ ,
Lizhang CHEN ¹ ,
Hong QIN ¹

Author information +

文章历史 +

PDF (650K)

摘要

黄精多糖是传统中药材黄精中的主要活性成分，呈现显著的结构异质性特征，糖链类型丰富，具有广泛的生物活性(包括抗炎、免疫调节、抗氧化、糖脂代谢调节等多重药理作用)，已成为医药健康领域研究与开发的热点方向。现代药理学研究表明：黄精多糖可通过调控核因子κB(nuclear factor kappa-B，NF-κB)、丝裂原活化蛋白激酶(mitogen-activated protein kinase，MAPK)、磷脂酰肌醇3激酶/蛋白激酶B(phosphatidylinositol 3-kinase/protein kinase B，PI3K/Akt)信号通路等多种途径，作用于炎症因子释放、免疫细胞活化、氧化应激反应、糖脂代谢等多个生物学靶点，从而发挥多靶点、多通路的协同效应。这一特性使其在预防和治疗炎症性疾病、代谢性疾病及癌症等领域展现出广阔的应用前景。尽管现有研究已在动物模型和体外实验中证实黄精多糖具有多种生物学活性，但其临床转化应用仍面临一定困难。未来研究应聚焦于结构-活性关系精准解析、体内代谢过程表征及循证医学证据获取，为推动黄精多糖从基础研究向临床应用转化提供科学依据。

Abstract

Polygonatum polysaccharides are the major active components of the traditional Chinese medicinal herb Polygonatum. They exhibit marked structural heterogeneity with diverse glycan types and possess a broad spectrum of biological activities, including anti-inflammatory, immunomodulatory, antioxidant, and glucose-lipid metabolic regulatory effects. These properties have made them a research hotspot in the fields of medicine and health. Modern pharmacological studies have shown that Polygonatum polysaccharides can modulate multiple biological targets by regulating several signaling pathways, such as nuclear factor kappa-B (NF-κB), mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt). Through these pathways, they influence inflammatory cytokine release, immune cell activation, oxidative stress responses, and glucose-lipid metabolism, thereby exerting synergistic multi-target and multi-pathway effects. This enables their promising application in the prevention and treatment of inflammatory diseases, metabolic disorders, cancers, and other conditions. Although numerous in vivo and in vitro studies have validated the wide-ranging biological activities of Polygonatum polysaccharides, challenges remain in their clinical translation. Future research should focus on the precise elucidation of structure-activity relationships, characterization of metabolic processes in vivo, and acquisition of rigorous evidence from clinical research to support the translation of Polygonatum polysaccharides from basic research to clinical application.

关键词

黄精多糖 / 生物学活性 / 抗炎 / 免疫调节 / 抗氧化剂 / 代谢调节

Key words

Polygonatum polysaccharides / biological activity / anti-inflammation / immunomodulation / antioxidant / metabolic regulation

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管佩瑶,李子业,王倩,丁涵,陈立章,秦虹. 黄精多糖的生物学活性及其在相关疾病防治中的作用[J]. 中南大学学报（医学版）, 2025, 50(9): 1664-1673 DOI:10.11817/j.issn.1672-7347.2025.250247

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黄精是中国传统药食两用的植物。黄精的法定来源包括3种：黄精(Polygonatum sibiricum Red.，又名鸡头黄精)、滇黄精(Polygonatum kingianum Coll.et Hemsl.，又名大黄精)和多花黄精(Polygonatum cyrtonema Hua，又名姜形黄精)，被广泛用于多种疾病的治疗。黄精多糖是指从黄精干燥根茎中提取分离得到的一类具有生物活性的多糖类大分子化合物^[1]，其组成结构复杂且具有显著的结构多样性特征。不同研究报告中黄精多糖的组成成分差异较大^[2]，这主要与选用黄精的品种、生长环境、成熟度及多糖的提取方法和分析程序不同有关。

在分子结构特征方面，黄精多糖分子量分布较宽，其分子量范围在5.1~322.0 kD(1 D=1 u)之间，目前已鉴定出37种特征性成分^[3-4]，不同分子量的多糖组分表现出差异化的生物活性。利用完全酸水解结合单糖衍生化技术，经高效液相色谱-荧光检测系统分析证实，黄精多糖单糖组成具有多样性，主要以果糖、葡萄糖、半乳糖、甘露糖等单糖为主，并含有少量的阿拉伯糖、岩藻糖、木糖、葡萄糖醛酸和半乳糖醛酸等^[5-6]。黄精多糖的糖链结构复杂，包括果聚糖型、果胶型、葡萄糖半乳甘露聚糖型、葡甘露聚糖型和阿拉伯半乳聚糖型等多种糖苷键连接类型^{[2, 7]}，形成具有分支结构的杂多糖。上述结构特征的多样性是黄精多糖发挥广泛生物活性的重要结构基础。黄精多糖在抗炎、调节免疫、抗氧化及调节糖脂代谢等方面具有多重功效。本文对近年来国内外黄精多糖生物学活性及其作用机制的研究进展进行综述，以期为黄精多糖的深入研究和开发提供理论参考，并推动其在医疗领域的深入应用和发展。

1 黄精多糖的抗炎及其对炎症相关疾病的防治作用

炎症是机体应对病原体感染、组织损伤或有害刺激的初级防御机制，其过度激活或持续发展可能导致急性炎症失控或慢性炎症迁延，进而引发全身炎症反应综合征甚至多器官功能障碍^[8]。黄精多糖的抗炎作用是其重要生物学活性之一，其作用机制涉及对多信号通路和分子靶点的调控，在多种炎症性疾病模型中表现出显著的组织保护效应。

急性炎症以中性粒细胞浸润、促炎因子暴发性释放为特征，黄精多糖能有效干预炎症级联反应的核心环节，通过抑制核因子κB(nuclear factor kappa-B，NF-κB)核转位及丝裂原活化蛋白激酶(mitogen-activated protein kinase，MAPK)磷酸化等关键分子事件，显著调节促炎-抗炎因子的动态平衡^[9-10]。在顺铂诱导的急性肾损伤模型大鼠^[11]中，黄精多糖通过下调p38 MAPK/活化转录因子2(activating transcription factor 2，ATF2)信号通路，显著抑制肿瘤坏死因子-α(tumor necrosis factor-alpha，TNF-α)、白细胞介素(interleukin，IL)-6及IL-1β等促炎因子表达，并促进抗炎因子IL-10释放，从而改善肾组织炎性浸润。在脂多糖诱导的急性肺损伤模型大鼠中观察到，黄精多糖可阻断Toll样受体(Toll-like receptor，TLR)4/髓样分化因子88(myeloid differentiation factor 88，MyD88)/NF-κB信号传导，使肺组织髓过氧化物酶活性降低，有效改善肺部病理损伤并减轻炎性浸润^[12]。Xiao等^[13]建立脓毒症急性肝损伤模型，发现黄精多糖通过抑制NOD样受体热蛋白结构域相关蛋白3(NOD-like receptor family pyrin domain containing 3，NLRP3)/消皮素D(Gasdermin D，GSDMD)信号通路减轻炎症反应来缓解小鼠急性肝损伤。基于定量蛋白质组学分析，该团队^[14]进一步证实黄精多糖对急性肝损伤的保护作用，表明其通过阻断NF-κB、IL-17、TNF-α及TLR等炎症信号通路发挥保肝作用。在心血管损伤模型中，黄精多糖能显著降低急性心肌梗死大鼠血清TNF-α、IL-6水平，同时下调心肌损伤标志物血清肌酸激酶同工酶-MB和乳酸脱氢酶活性，有效减轻心肌组织炎性损伤^[15]。黄精多糖的多靶点调控机制为抗炎治疗提供了科学依据。

慢性炎症以促炎因子持续释放、炎症细胞异常浸润为特征，黄精多糖可通过直接干预炎症信号通路的活化与传导，表现出对炎症的持续调控能力。研究^[16]发现黄精多糖通过阻断核因子κB抑制激酶β(inhibitor of nuclear factor kappa-B kinase beta，IKKβ)磷酸化并抑制NF-κB核转位，可有效缓解IL-1β诱导的软骨细胞炎症。有学者^[17]建立了膝骨关节炎小鼠模型，发现黄精多糖可有效抑制小鼠膝关节软骨中TLR2/NF-κB信号通路，降低血清中炎症因子水平，显著减缓骨关节炎的病理进程。有证据^[18]指出黄精多糖可抑制神经系统中星形胶质细胞活化，通过调节NF-κB依赖的炎症途径有效控制神经炎症发展。在妊娠相关炎症模型^[19]中，黄精多糖可降低大鼠胎盘IL-6、TNF-α等炎症因子含量，提升抗炎因子IL-10含量，减轻妊娠期慢性炎症反应。黄精多糖对炎症信号通路的持续调控作用，为慢性炎症疾病的长期管理开辟了新途径。

黄精多糖的抗炎作用主要是通过调控NF-κB等多种信号通路及下游分子靶点，将炎症因子水平控制在生理范围内，在急性与慢性炎症模型中均表现出显著的组织保护作用。其作为天然药物在辅助治疗炎症性疾病、减轻组织损伤中具有重要潜力。

2 黄精多糖的免疫调节及其对免疫相关疾病的防治作用

免疫系统是机体维持稳态的核心防线，其功能失衡可导致免疫抑制、感染性疾病或自身免疫病，严重威胁人体健康。黄精多糖是一类具有免疫调节活性的植物化学物，毒性及不良反应较小，可通过促进免疫器官发育、调节免疫细胞数量和功能等方式，构建免疫稳态调节网络。

固有免疫系统是机体应对外界刺激的第一道关键防线，也是激活适应性免疫的重要步骤。当机体免疫功能低下时，会导致抗感染和疾病防御能力下降，增加罹患免疫相关疾病的风险。动物实验^[20]表明黄精多糖可通过改善免疫器官微环境发挥系统调节作用。在血虚综合征模型小鼠中，黄精多糖可以防止血虚综合征引起的脾脏萎缩，并将脾脏的所有结构特征恢复至正常水平，进一步的转录组学分析显示其可能通过激活免疫细胞、促进细胞因子分泌等机制改善免疫抑制。Chen等^[21]建立环磷酰胺诱导的免疫抑制小鼠模型，发现黄精多糖不仅增加了脾脏与胸腺的器官指数，还促进了淋巴细胞的增殖，并正向调节了细胞因子，从而为机体构建稳固的免疫防御机制。在免疫细胞调控层面，黄精多糖展现出病理状态适应性调节特征。黄精多糖通过剂量依赖性激活巨噬细胞、增强自然杀伤细胞活性及促进T细胞亚群增殖等方式，有效增强机体抗病原体感染的能力。具体表现为，黄精多糖可以促进巨噬细胞的增殖，并增强其通过吞噬死亡细胞和病原体等物质来维持免疫稳态的能力^[22]。黄精多糖在RAW264.7巨噬细胞模型中展现出显著的体外免疫调节活性，其通过激活TLR4/NF-κB信号通路，促进巨噬细胞吞噬功能及适度炎症因子的释放，增强免疫监视^[23-27]。研究^[28]发现：黄精多糖能增加小鼠外周白细胞、淋巴细胞及粒细胞的数量，并提高自然杀伤细胞活性来增强免疫抑制小鼠的免疫力。黄精多糖不仅能直接刺激免疫细胞的增殖与功能，还能促进一氧化氮及多种关键细胞因子(如IL-6、IL-1β、IL-10、IL-12等)的释放，上调诱导型一氧化氮合酶(inducible nitric oxide synthase，iNOS)的表达水平，通过发挥非特异性免疫调节功能，增强巨噬细胞的吞噬作用和自然杀伤细胞的杀伤能力，进一步激活了免疫应答的级联反应^[29]。此外，黄精多糖可促进非特异性免疫防御因子溶血素的生成^[30]及免疫球蛋白(immunoglobulin，Ig)G/IgM抗体生成^[28]，形成“固有免疫-适应性免疫”的防御体系。在免疫调节机制中，自身免疫疾病因免疫耐受失衡引发异常攻击自身组织，辅助性T(helper T，Th)17细胞/调节性T(regulatory T，Treg)细胞的失衡是核心病理环节。Th17细胞给予机体免疫刺激，而Treg细胞会抑制自身免疫。黄精多糖可调节Th17/Treg平衡向Treg倾斜^[31]，并可调节小鼠的全身免疫反应并恢复免疫稳态^[32]。以上证据表明黄精多糖通过“器官-细胞-分子”三级调控体系发挥免疫调节作用。

黄精多糖能增强机体的调节免疫能力，通过“器官重塑-细胞激活-分子调控”三级作用网络，在免疫缺陷、感染性疾病及免疫衰老等病理过程中展现出治疗潜力。

3 黄精多糖的抗氧化及其对氧化损伤疾病的防治作用

氧化应激是机体活性氧(reactive oxygen species，ROS)生成与清除系统失衡导致的病理状态，其引发的生物大分子及信号通路异常激活，可加速氧化损伤相关疾病的进展。近年研究证实黄精多糖可通过多靶点调控氧化还原稳态，在氧化损伤模型中发挥显著的保护效应。

当机体中自由基的生成速率超过抗氧化防御系统的清除能力时，会引发细胞功能障碍或组织损伤。黄精多糖能够直接清除体内的羟基自由基、超氧阴离子自由基等多种自由基，主要通过2种途径发挥抗氧化功效：一方面，它能够直接抑制一氧化氮(nitric oxide，NO)、NOS、ROS、丙二醛(malondialdehyde，MDA)等氧化应激产物的产生，缓解氧化应激损伤；另一方面，它还可以调节抗氧化酶活性，阻止NO及NOS与氧自由基的结合，降低细胞的氧化损伤^{[7, 33-35]}。体外自由基清除实验^[36]显示：低分子量黄精多糖易于接近并中和2,2’-联氮基双-(3-乙基苯并噻唑啉-6-磺酸)自由基，有效阻断自由基链式反应；而高分子量黄精多糖则具有更多的活性位点，能清除1,1-二苯基-2-三硝基苯肼自由基。研究^[33]发现：黄精多糖可以降低小鼠体内ROS和MDA水平，同时增加了D-gal处理小鼠心脏中超氧化物歧化酶(superoxide dismutase，SOD)的水平，并抑制氧化应激引起的DNA损伤和脂质过氧化。同样，在D-gal诱导的氧化损伤小鼠^[37]中，黄精多糖能够降低Kelch样环氧氯丙烷相关蛋白-1(Kelch-like epichlorohydrin protein-1，Keap1)的表达来增强核转录因子红系2相关因子2(nuclear factor-erythroid 2-related factor 2，Nrf2)的活性，促进血红素加氧酶1(heme oxygenase-1，HO-1)等抗氧化酶的合成，从而增强机体的抗氧化能力。黄精多糖还有改善小鼠帕金森行为并保护多巴胺能神经元免于死亡的潜力，而多巴胺能神经元退化与氧化应激增加和神经元氧化还原稳态破坏有关，这可能是黄精多糖通过蛋白激酶B(protein kinase B，Akt)/哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin，mTOR)介导的抗凋亡和Nrf2调节的抗氧化途径发挥神经保护作用^[38-39]。Debnath等^[40]利用H₂O₂诱导的肝细胞氧化损伤模型，发现黄精多糖能够显著降低肝细胞中总ROS水平，且呈剂量依赖性。其机制可能是通过激活沉默信息调节因子1(silence information regulator 1，SIRT1)/腺苷酸活化蛋白激酶(adenosine monophosphate-activated protein kinase，AMPK)/过氧化物酶体增殖物激活受体(peroxisome proliferator-activated receptor，PPAR)γ的辅激活因子α信号通路，调控线粒体生物合成，增强机体抗氧化应激能力，来缓解细胞的氧化损伤^[41]。黄精多糖还可显著减轻铀暴露所致的HK-2肾小管上皮细胞氧化应激损伤，具体机制可能与调节糖原合成酶激酶-3β(glycogen synthase kinase-3 beta，GSK-3β)/原癌基因酪氨酸蛋白激酶(proto-oncogene tyrosine-protein kinase，Fyn)/Nrf2通路有关^[42]。研究人员^[43]在此基础上利用铀诱导的肾脏损伤大鼠进一步验证黄精多糖的抗氧应激效应，结果显示黄精多糖干预可显著降低血清肌酐和尿素氮水平，并通过激活Nrf2介导的抗氧化防御系统，上调SOD和谷胱甘肽过氧化物酶(glutathione peroxidase，GSH-Px)活性，同时降低了MDA含量。上述证据证实了黄精多糖在氧化损伤疾病防护中的调控优势。

综上，黄精多糖通过直接清除自由基、激活内源性抗氧化防御系统等机制，在预防和治疗氧化损伤疾病中发挥关键作用。

4 黄精多糖的糖脂代谢调节及其对代谢紊乱疾病的防治作用

糖脂代谢紊乱是糖尿病、肥胖症及动脉粥样硬化等常见代谢性疾病的共同病理基础，其特征包括胰岛素抵抗、脂质异位沉积等。黄精多糖在糖脂代谢调控方面表现出显著的生物学活性，具体机制涉及糖脂代谢关键酶活性调节、胰岛素信号通路激活及糖脂代谢相关基因表达调控等。

黄精多糖可通过胰岛保护与外周组织协同调节糖代谢。在胰腺组织中，黄精多糖能抑制胰岛细胞的凋亡，并通过改善链脲佐菌素(streptozotocin，STZ)导致的自由基损伤和胰腺免疫损伤来维持胰岛正常功能，改善胰岛素抵抗，进而维持血糖稳定^[44]。研究^[45]显示：黄精多糖通过竞争性抑制α-葡萄糖苷酶和α-淀粉酶活性，来延缓碳水化合物分解，减少餐后血糖波动。在外周组织中，黄精多糖促进细胞对葡萄糖的摄取和利用，增加胰岛素敏感性，从而降低空腹血糖。黄精多糖激活磷脂酰肌醇3激酶(phosphatidylinositol 3-kinase，PI3K)/Akt信号通路，促进骨骼肌和脂肪细胞对葡萄糖的摄取^[46]。Chen等^[47]的研究还发现，黄精多糖可上调己糖激酶活性，促进糖酵解，同时下调磷酸烯醇式丙酮酸羧激酶和葡萄糖-6-磷酸酶的表达，抑制肝糖异生，实现血糖稳态调控^[48]。黄精多糖多靶点调控糖代谢关键环节的特性，为糖尿病防治提供了整合性干预策略。

黄精多糖在降脂方面也具有显著效果，其可与脂质代谢相关的相应基因和蛋白质相互作用，从而对降低血脂起到关键作用。研究^[49]显示黄精多糖能降低高脂血症模型动物血清中的总甘油三酯(triglyceride，TG)和总胆固醇(total cholesterol，TC)含量，其降脂机制主要涉及脂肪的合成与分解过程。具体而言，黄精多糖能够直接抑制脂肪酸合成酶的活性，阻断脂肪酸生物合成途径，从而减少TG生成^[50-51]；同时显著增强激素敏感性脂肪酶的活性，促进脂肪组织水解过程^[52]，其具体机制与AMPK/PPAR信号通路的激活密切相关。孔瑕等^[53]通过建立高脂血症小鼠模型，发现不同剂量黄精多糖均显著降低小鼠血清中TC、TG及低密度脂蛋白胆固醇含量，该作用可能通过调控PPAR通路实现：一方面上调PPAR-α、PPAR-β的表达以促进脂肪酸β-氧化；另一方面下调PPAR-γ、固醇调节元件结合蛋白(sterol regulatory element-binding protein，SREBP)1c的表达，从而抑制脂肪细胞分化。黄精多糖还可通过肠道-代谢轴调控脂代谢，其能修复肠道屏障^[54]，有效抑制脂多糖入血，从而预防脂质代谢紊乱^[55-56]。除基础降脂作用外，黄精多糖还展现出显著的心血管保护特性。在动脉粥样硬化模型^[57-59]中，黄精多糖能够降低血脂水平，改善主动脉形态，减少泡沫细胞形成，并保护内皮细胞功能，以及降低斑块面积和脂质沉积，来发挥抗动脉粥样硬化作用。在STZ联合高脂饮食诱导的Ⅱ型糖尿病模型^[60]中，黄精多糖显示出代谢综合征的协同治疗效果，其通过激活PI3K/Akt信号轴同步改善胰岛素抵抗与高脂血症。黄精多糖通过脂质合成-分解平衡调控及肠道屏障保护，构建脂代谢稳态维持的系统性解决方案。

黄精多糖能维护糖脂代谢平衡，其作用涵盖酶活性抑制、信号通路激活、基因表达调控等多重机制。因此，黄精多糖在预防和治疗糖尿病、肥胖等代谢性疾病方面展现出较好的应用前景。

5 黄精多糖的其他作用

黄精多糖可通过调节肠道菌群的结构和功能发挥健康效应：一方面促进乳酸菌、双歧杆菌等有益菌的增殖，抑制大肠杆菌等致病菌的定植；另一方面提升短链脂肪酸的产生，有效改善肠道健康^[49]。这种菌群调控效应可能对全身代谢平衡产生积极影响，通过“肠-器官轴”影响其他组织疾病进程。研究^[61-64]表明：黄精多糖可调节肠道微生物群结构，激活小胶质细胞的吞噬功能，增加β淀粉样蛋白斑块的清除效率，从而改善阿尔茨海默病模型小鼠的认知功能障碍。

黄精多糖还可对细胞周期进行精准调控，来动态平衡细胞周期进程。研究^[65-67]表明：黄精多糖通过调节p53/p21等细胞周期相关基因解除周期阻滞，促进骨髓间充质干细胞增殖并抑制凋亡通路。此外，黄精多糖还可增强C2C12成肌细胞活力并促进肌管分化。这证实了黄精多糖在创伤修复应用中的细胞学基础。黄精多糖还可选择性阻滞肿瘤细胞G₁期和G₂/M期进程，抑制周期蛋白依赖性激酶1(cyclin-dependent kinase 1，CDK1)/细胞周期蛋白B1(cyclin B1)等周期调控蛋白活性来发挥抗肿瘤作用^[68-69]。此外，在骨骼系统研究^{[34, 70]}中，黄精多糖通过调节骨钙素信号通路及Klotho-FGF23轴动态平衡，显著改善钙磷代谢紊乱来延缓骨组织退行性病变，为防治骨质疏松等退行性骨病提供了新思路。

黄精多糖通过多靶点、多通路机制，在肠道菌群调控、细胞周期调节等领域发挥广泛的生物活性。这种多维度的功能特性不仅展现了其作为功能性食品成分的科学基础，还为开发新型营养干预策略提供了重要理论支撑。

黄精多糖的主要生物学活性及其作用机制总结见表1。

6 结语与展望

黄精多糖因其独特的分子结构和多元化的生物活性，近年来在医药健康领域受到广泛关注，其主要生物学活性已通过大量体内外研究得到验证。目前已有针对黄精多糖纯化组分进行生物活性研究的报道，但现有研究主要集中在黄精多糖粗提物的生物学效应，包括其在抗炎、免疫调节、抗氧化及糖脂代谢调节等方面在动物细胞模型中的初步验证。黄精多糖在构效关系、多靶点作用网络构建及临床转化研究等方面仍待深入探索。

在未来的研究中，可进一步利用核磁共振、质谱等高级分析技术，明确黄精多糖糖链分支模式与活性位点，构建结构-活性定量模型；结合多组学技术，全面解析黄精多糖多效性的分子网络，揭示其发挥作用的深层机制；推进多中心临床试验，全面评估黄精多糖在防治人类疾病中的长期安全性、有效性和药代动力学特性，为其临床应用提供循证医学证据。通过整合多学科资源和技术手段，黄精多糖有望在健康促进和疾病防治领域发挥更大的作用。

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