Research Progress on the Protective Effects of Active Components of Huangqi (Astragali Radix) on Pancreatic β-Cells

Abstract

The potential application of Huangqi (Astragali Radix) in the treatment of diabetes mellitus (DM) has garnered increasing attention. β-cell dysfunction is one of the core mechanisms in the pathogenesis of DM and effectively protecting and restoring pancreatic β-cell function remains a key challenge in DM prevention and treatment. Studies have shown that the active components of Huangqi (Astragali Radix) can alleviate glucolipotoxicity-induced β-cell damage by promoting glucose uptake mediated by glucose transporter 4 (GLUT-4), inhibiting the Wnt1/β-catenin signaling pathway to reduce lipid deposition in liver and pancreatic tissues and upregulating peroxisome proliferator-activated receptor α (PPARα) gene expression. Additionally, Huangqi (Astragali Radix) can reduce cell apoptosis by mitigating endoplasmic reticulum stress, suppress pyroptosis via the NF-κB/NLRP3/TXNIP signaling pathway, and inhibit ferroptosis and autophagy to decrease β-cell death. Furthermore, Huangqi (Astragali Radix) can promote β-cell proliferation by modulating dedifferentiation and transdifferentiation, improve the islet microenvironment by regulating immune function and reducing M1 macrophage polarization, and may delay β-cell senescence. This review summarizes the research progress of active ingredients in Huangqi (Astragali Radix) in protecting pancreatic β-cell, which provides new insights and a scientific basis for its future application in DM prevention and treatment.

 

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Keywords

Huangqi - Astragali Radix - pancreatic β-cells - diabetes mellitus - glucose and lipid metabolism - cell death - senescence

Huangqi (Astragali Radix), a traditional Chinese medicinal herb with a long history of use, was first documented in the Shennong's Classic of Materia Medica (Shen Nong Ben Cao Jing). Its primary active components—including astragalus polysaccharides (APS), flavonoids, saponins, and alkaloids—endow it with diverse pharmacological properties, such as immunomodulation, antioxidation, and antitumor effects.[1] Notably, Rihuazi's Materia Medica (Ri Hua Zi Ben Cao) records its efficacy in treating “consumptive thirst.” In recent years, against the backdrop of rising global diabetes mellitus (DM) prevalence,[2] researchers have increasingly explored the therapeutic potential of Huangqi (Astragali Radix) in treating DM. Pancreatic β-cell dysfunction is a central mechanism in DM pathogenesis, making the protection and functional restoration of β-cells a persistent focus and challenge in DM prevention and treatment. This encompasses not only the protection of β-cells themselves but also the improvement of their metabolic microenvironment, promotion of regeneration, and delay of senescence, all aimed at restoring their insulin-secreting capacity. Such comprehensive approaches enable effective glycemic control and reduce the risk of DM-related complications. Consequently, investigating the protective role of Huangqi (Astragali Radix) and its active components in β-cell preservation holds significant clinical value and application prospects.

Mitigation of Glucolipotoxicity

Prolonged exposure to elevated glucose and lipid levels induces glucolipotoxicity, which can directly or indirectly damage pancreatic β-cells through oxidative stress (OS), endoplasmic reticulum stress (ERS), and inflammatory responses, ultimately contributing to the development of DM.[3] Glucolipotoxicity also impairs insulin gene transcription and significantly reduces the binding affinity between insulin gene sequences and pancreatic and duodenal homeobox factor 1 (PDX-1).[4] Studies have shown that in a high-fat environment, elevated free fatty acid (FFA) levels downregulate the expression of glucose transporter 2 (GLUT-2) on β-cells, thereby impairing insulin secretion.[5] Under persistent hyperglycemic conditions, β-cells may adapt through mechanisms such as abnormal calcium signaling and suppression of the phospholipase C pathway, leading to glucose desensitization.[6]

Research indicates that APS inhibits the Wnt1/β-catenin signaling pathway, upregulates the expression of fatty acid synthase and lipoprotein lipase in the liver and pancreas of mice, reduces lipid deposition, and alleviates β-cell damage.[7] Wang and Lin[8] have found that long-term APS administration in a DM mouse model can significantly lower blood glucose and body weight, enhance the expression of GLUT4 and glycogen synthase kinase-3β (GSK-3β) in pancreatic tissues, increase insulin and adiponectin levels, and protect β-cells. Additionally, APS exerts antioxidant effects by upregulating nuclear factor erythroid 2-related factor 2 (Nrf2), glutamate-cysteine ligase catalytic subunit, heme oxygenase-1 (HO-1), and catalase, thereby ameliorating glucolipid metabolic disorders.[9] Xiao[10] demonstrated that astragaloside IV (AS-IV) directly reduces glucose and lipid levels by modulating the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) and AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1) signaling pathways. By increasing serum adiponectin levels, astragalosides II and isoastragaloside I enhance GLUT-4-mediated glucose uptake, suppress proinflammatory cytokine transcription, alleviate inflammation, improve insulin resistance (IR), and protect β-cells.[11] qRT-PCR analysis revealed that AS-IV reduces the expression of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in adipocytes while significantly upregulating GLUT-4, directly mitigating β-cell toxicity.[12] Furthermore, total flavonoids of astragalus (TFA) increase the expression of peroxisome proliferator-activated receptor α (PPARα),[13] and the activated PPARα lowers plasma triglyceride (TG) and low-density lipoprotein cholesterol, elevates high-density lipoprotein cholesterol, thereby improving dyslipidemia.

 

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Reducing Pancreatic β-Cell Death

Inhibiting Apoptosis

Extensive research has confirmed that both type 1 diabetes mellitus and type 2 diabetes mellitus (T2DM) involve β-cell apoptosis. As a type I programmed cell death mechanism, apoptosis is highly complex and can be induced by various factors, including inflammatory stimuli, ERS, OS, islet amyloid polypeptide (IAPP), gut microbiota dysbiosis, alterations in the islet microenvironment, mitochondrial dysfunction,[14] and overexpression of miR-126.[15] A recent study revealed that the bile acid farnesoid X receptor (FXR)-lysine (K)-specific demethylase 6A (KDM6A)-gamma-aminobutyric acid B receptor subunit 1 (Gabbr1) axis enhances β-cell survival by reducing apoptosis.[16] In Min6 cells, palmitic acid (PA)-induced ERS upregulates marker proteins such as phosphorylated protein kinase R-like endoplasmic reticulum kinase (p-PERK), activating transcription factor 4 (ATF4), glucose-regulated protein 78 (GRP78), and the apoptosis marker protein CCAAT/C/EBP homologous protein (CHOP). The cascade reaction of cysteine-dependent aspartate-specific protease (Caspase) family induces cell apoptosis.[17]

In the process of β-cell apoptosis, APS can reduce the accumulation of glucose and lipids in the pancreas through the AMPK metabolic pathway, interfere with the Fas/Fas-L system and the expression of Caspase-3, upregulate the expression of B-cell lymphoma 2 (Bcl-2), and inhibit the mitochondrial death pathway mediated by the pro-apoptotic protein Bcl-2 associated X protein (Bax).[18] Wu et al[7] demonstrated that APS's anti-apoptotic effects may be linked to ERS alleviation, as long-term APS administration normalized endoplasmic reticulum folding and significantly reduced apoptosis rates in pancreatic tissues. Wang et al[19] found that AS-IV dose-dependently modulates CHOP expression induced by the inositol-requiring enzyme 1 (IRE1), PERK, and activating transcription factor 6 (ATF6) pathways, which attenuates downstream pro-apoptotic signals and decreases apoptosis rates. Furthermore, AS-IV reduces NADPH Oxidase 4 (NOx4) overexpression, ameliorates OS, and suppresses apoptosis. Modern pharmacological studies have shown that TFA exhibits potent antioxidant, anti-inflammatory, and free radical-scavenging properties. Among these, calycosin (CAL) demonstrates the most significant antioxidant activity.[20] Its phenolic hydroxyl groups react with free radicals, which terminates chain reactions while upregulates the activities and expression of antioxidant enzymes, catalase, and superoxide dismutase, thereby alleviating OS and improving β-cell function. Research has discovered that TFA's efficacy in ameliorating IR surpasses that of APS and other astragalus monomers, potentially due to its ability to enhance aminopeptidase N activity and elevate serum insulin levels.[8] In DM rat models, TFA increases AMPK mRNA and AMPK expression, thus reducing reactive oxygen species (ROS) accumulation. Through indirect regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity, AMPK further exerts antioxidant effects,[13] ultimately protecting β-cells from apoptosis.

 

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Suppressing Pyroptosis

Studies have demonstrated that excessive cellular activation-induced proinflammatory responses can trigger pyroptosis, thereby influencing the progression of DM. In T2DM mouse models, advanced glycation end products-induced hyperglycemia and pancreatic cell damage activate the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome. NLRP3 gene knockout has been shown to enhance insulin secretion.[21] Additionally, high-glucose stimulation can induce NLRP3-mediated pyroptosis by suppressing β-cell autophagy.[22] Increased expression of cysteine-dependent aspartate-specific protease-1 (caspase-1) further exacerbates islet injury. These findings indicate that pyroptosis contributes to β-cell damage, impairs insulin secretion, and promotes IR. In vitro experiments revealed that the miR-322-5p gene alleviates β-cell pyroptosis and improves insulin secretion by targeting programmed cell death protein 4 (PDCD4) to activate the PI3K/AKT pathway.[23] Therefore, investigating the regulatory effects of active components of Chinese medicine on pyroptosis holds significant potential for β-cell protection.

Active components of Chinese medicine modulate pyroptosis-related pathways through multiple mechanisms. Under hyperglycemic conditions, AS-IV amplifies OS responses and activates NLRP3, leading to elevated inflammatory cytokine levels and subsequent pyroptosis. Astragaloside I reduces serum concentrations of interleukin-1β (IL-1β) and interleukin-18 (IL-18) in db/db mice while downregulating pyroptosis-related markers such as NLRP3, Caspase-1, and gasdermin-N terminal domain (GSDMD-N).[24] Through the p65 NF-κB/NLRP3/TXNIP signaling pathway in SD rats, CAL inhibits NF-κB activation, reduces thioredoxin-interacting protein (TXNIP) expression, and suppresses the secretion of inflammatory factors including NLRP3, IL-1β, and interleukin-10 (IL-10), thereby mitigating β-cell pyroptosis.[25] Ozamj et al[26] reported that formononetin significantly lowers blood glucose, total cholesterol (TC), TG, and plasma insulin levels in T2DM mice and improves IR, and upregulates sirtuin 1 (SIRT1) expression in pancreatic tissues, suggesting its protective role of β-cell against oxidative damage in DM. The underlying mechanism may involve SIRT1-mediated inhibition of mitochondrial uncoupling protein 2 (UCP2) activity, which subsequently modulates glucose and lipid metabolism. Collectively, these findings highlight that flavonoids derived from Huangqi (Astragali Radix) can regulate key signaling pathways to attenuate inflammatory responses and provide a more stable microenvironment for β-cell survival.

 

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Inhibiting Ferroptosis

Ferroptosis, an emerging form of cell death, is associated with polyunsaturated fatty acid peroxidation and iron accumulation, leading to cellular damage.[27] [28] Studies have shown that pancreatic β-cells are particularly vulnerable to OS, which increases ROS production and downregulates glutathione peroxidase 4 (GPX4) expression, triggers ferroptosis, and impairs β-cell function.[29] In T2DM mouse models, ferroptosis induces characteristic pathological changes in β-cell mitochondria and overall structure.[30] Inhibiting the ubiquitin-proteasome pathway of GPX4 has been shown to reduce ferroptosis and preserve β-cell function.[31] Further analysis revealed that this protective effect correlates with the expression of iron metabolism-related proteins, such as increased levels of ferritin and transferrin receptors in treated groups. Additionally, the ferroptosis inhibitor ferrostatin-1 has been demonstrated to effectively mitigate β-cell damage, highlighting the potential significance of ferroptosis in DM pathogenesis. Thus, ferroptosis inhibitors can upregulate GPX4 expression, reduce lipid peroxidation, and prevent ferroptosis.[32]

Targeting ferroptosis presents a novel therapeutic perspective for DM. Research indicates that certain natural polysaccharides can regulate iron homeostasis and reduce systemic iron overload. For instance, APS upregulates hepcidin expression by promoting interleukin-6 (IL-6) release and activating the p38 MAPK signaling pathway.[33] AS-IV may suppress macrophage ferroptosis and lipid deposition by downregulating tumor protein 53 (P53) while enhancing the expression of ferritin heavy chain (FTH1), solute carrier family 7 member 11 (SLC7A11), and GPX4 at both protein and gene levels. CAL reduces lactate dehydrogenase, malondialdehyde, and lipid ROS levels while boosting glutathione (GSH) activity and GPX4 expression, thereby inhibiting ferroptosis.[34] Among Astragalus flavonoids, quercetin has shown potential to mitigate pancreatic iron deposition, ameliorate mitochondrial atrophy and cristae loss in T2DM mice, and preserve islet morphology and structure. Iron chelators can modulate mitochondrial adenosine triphosphate (ATP) synthesis, reduce ROS production, and activate the HIF-1α/HO-1 pathway, improve insulin secretion and glucose tolerance.[29] As a natural iron chelator,[35] quercetin lowers ferritin levels, upregulates GSH and GPX4 expression, reverses iron overload, and restores β-cell function.[36] Feng et al[37] [38] demonstrated that quercetin's anti-ferroptotic effects involve GPX4 and the Nrf2/heme oxygenase-1 (HO-1), which can downregulate GPX4 expression, increase FTH1, decrease transferrin receptor-1 expression. Current studies primarily detect ferroptosis through indirect indicators such as ROS levels, lipid peroxidation products, iron concentrations, and GPX4 activity.

 

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Suppressing Autophagy

Autophagy, a type II programmed cell death mechanism, serves as a critical self-protective process in organisms. It involves the fusion of autophagosomes with lysosomes to form autolysosomes, where cellular components are degraded by acidic proteases and recycled.[39] Studies indicate that pancreatic β-cells exhibit significantly higher sensitivity to autophagy than α-cells. However, under conditions such as OS, inflammation, ERS,[40] elevated homocysteine levels,[41] excessive FFA,[42] autoimmune damage, or dysregulated autophagy (either insufficient or excessive),[43] aberrant autophagy can impair β-cell function. For instance, mice with autophagy-related gene 7 (Atg7) deficiency exhibit β-cell degeneration, reduced insulin secretion, and impaired glucose tolerance.[44] Research also suggests that oscillating high glucose levels disrupt β-cell function and viability by inducing mitophagy via the PI3K/Akt/mammalian target of rapamycin (mTOR) pathway.[45] Kim et al[46] demonstrated that autophagy clears IAPP oligomers and suppresses oligomer-mediated β-cell apoptosis. Additionally, PDX-1 protects β-cells by inhibiting autophagosome-lysosome fusion during autophagy initiation.[43] Moderate OS activates the PINK1-PARKIN pathway and promotes ubiquitination of mitochondrial outer membrane proteins and subsequent degradation via proteasomal and autophagic clearance of damaged mitochondria. Nevertheless, balanced autophagy is essential for maintaining cellular homeostasis and normal β-cell function,[47] highlighting its dual role in β-cell survival.

Modulating autophagic flux is pivotal for β-cell protection. Studies reveal that AS-IV ameliorates OS and hyperinflammatory responses under high-glucose conditions and preserves cellular function.[48] This effect may involve suppression of the NLRP3 inflammasome pathway, reduction of pro-inflammatory cytokines, and upregulation of autophagy to eliminate harmful cellular components and reduce excessive inflammatory responses. Among Astragalus flavonoids, quercetin mitigates OS, restores lysosomal function, and reduces β-cell apoptosis. Its mechanism includes promoting degradation of microtubule-associated protein 1 light chain 3-II (LC3-II) and sequestosome-1 (p62) in β-cells and rat islets, thereby alleviating autophagosome accumulation and autophagic flux blockade.[49] Concurrently, quercetin inhibits lysosomal membrane permeabilization and prevents cathepsin leakage into the cytosol and lysosomal vesicle dysfunction, ultimately improving β-cell survival. Precise regulation of autophagic flux thus represents a promising strategy to balance β-cell viability and death.

 

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Modulating β-Cell Dedifferentiation and Transdifferentiation

Research has revealed that dedifferentiation is a critical mechanism contributing to pancreatic β-cell dysfunction. β-cell dedifferentiation refers to the process by which mature β-cells lose their functional markers (e.g., insulin, PDX1) and may acquire progenitor or other endocrine cell characteristics, which plays a significant role in DM pathology.[50] Neelankal et al[51] demonstrated the association between β-cell dedifferentiation and chronic hyperglycemia, noting reduced expression of dedifferentiation-specific transcription factors including PDX1, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA). Under conditions of OS, ERS, inflammation, hypoxia, lipotoxicity, or prolonged hyperglycemia,[52] β-cell populations undergo dynamic changes, leading to functional “exhaustion” and “dormancy,” and impairing normal insulin secretion. Studies report that anti-inflammatory therapies targeting IL-1β, TNF-α, or NF-κB can restore β-cell's islet secretory function in mice and prevent pathological dedifferentiation.[53] β-cell transdifferentiation involves the conversion of β-cells into other endocrine cell types under specific conditions, resulting in loss of β-cell functional and morphological characteristics. Accili[54] found that forkhead box protein O1 (FoxO1) deficiency in mouse models triggered dedifferentiation, characterized by downregulation of PDX1, MafA, NKX6.1, and GLUT-2, alongside upregulation of embryonic transcription factors like neurogenin 3 (Ngn3), octamer-binding transcription factor 4 (Oct4), and nanog homeobox (Nanog), ultimately driving transdifferentiation into non-β-cell lineages. Experiments confirm that FFAs suppress PDX1 expression and promote β-to-α-cell transdifferentiation.[55] This process is reversible; transplantation of bone marrow mesenchymal stem cells from T2DM patients into db/db mice demonstrated β-cell reversibility and improved glucose homeostasis.[56] Thus, under extreme β-cell loss, pancreatic non-β-cells or even hepatic cells may transdifferentiate into functional β-cells, thus increasing the number of cells and restoring islet function.

Recent studies have explored Chinese medicine through a modern biological lens to uncover its effects on β-cell dedifferentiation/transdifferentiation. Integrative approaches reveal that certain herbal components can activate specific pathways to promote β-cell proliferation and suppress dedifferentiation. For instance, CAL from Huangqi (Astragali Radix) downregulates expressions of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) in a dose-dependent manner, thus inducing endothelial transdifferentiation.[57] Similarly, tanshinone from Danshen (Salviae Miltiorrhizae Radix et Rhizoma) inhibits high glucose-induced β-cell dedifferentiation while enhancing proliferation. These findings highlight how dedifferentiation/transdifferentiation mechanisms offer novel therapeutic perspectives and bridge Traditional Chinese Medicine principles with contemporary biology to innovate DM treatment strategies.

 

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Immunomodulation

Macrophages play a pivotal role in nonspecific immunity. In patients with T2DM, increased macrophage infiltration within pancreatic islets leads to elevated secretion of proinflammatory cytokines such as TNF-α and IL-6, which subsequently impair β-cell function. Under hyperglycemic conditions, human islets are stimulated to secrete damage-associated molecular patterns, which further promote macrophage recruitment into islets. This process exacerbates local inflammation and accelerates β-cell apoptosis.[58] Deficiency of hypoxia-inducible factor-1α (HIF-1α) in macrophages ameliorates adipose tissue inflammation and IR.[59] Under metabolic stress, IAPP deposition or high-fat conditions, macrophage maturation shifts toward a proinflammatory M1 phenotype while suppressing anti-inflammatory M2 polarization. This imbalance enhances islet antigen presentation to CD4⁺T cells and triggers autoimmune attacks against β-cells.[60] Increased M1 macrophage accumulation in T2DM islets underscores the intricate link between islet inflammation and DM pathogenesis.

Investigating Chinese medicine-mediated macrophage polarization offers novel strategies for β-cell protection. Studies indicate that AS-IV exhibits potent anti-inflammatory properties by reducing M1 macrophage-derived cytokines, rectifying immune dysfunction, and mitigating β-cell damage, thereby remodeling the islet microenvironment. The anti-inflammatory mechanism of AS-IV involves suppression of NF-κB signaling to inhibit inflammatory mediator release. Wang et al[61] demonstrated that TFA modulates NF-κB-dependent transcription of inflammatory factors, attenuates LPS-induced excessive transcription of proinflammatory cytokines and their mRNAs in RAW264.7 cells, thus achieving dual anti-inflammatory and immunoregulatory effects. TFA also enhances immune responses in vitro[62] by promoting RAW264.7 macrophages to secrete IL-6, IL-1β, IFN-γ, TNF-α, nitric oxide (NO), prostaglandin E2 (PGE2), and upregulating inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). CAL suppresses T-cell proliferation and macrophage cytotoxicity, exhibiting combined anti-inflammatory and immunosuppressive actions.[26] Quercetin ameliorates white adipose tissue inflammation-induced insulin signaling dysfunction by decreasing macrophage infiltration in white adipose tissue, inhibiting M1 while promoting M2 macrophage polarization, and reducing expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6).[63] These findings illuminate the potential of Huangqi (Astragali Radix)-derived compounds in immunomodulation for DM therapy.

 

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Delaying Pancreatic β-Cell Senescence

In metabolic disorders such as DM, persistent hyperglycemia, chronic or excessive inflammatory responses, and lipotoxicity contribute to OS-mediated damage in pancreatic β-cells, accelerate their senescence and apoptosis, ultimately leading to reduced cell mass and functional decline. Studies indicate that alterations in the growth hormone/insulin-like growth factor-1 (IGF-1) axis significantly influence cellular senescence. While short-term IGF-1 exposure stimulates cell proliferation, prolonged IGF-1 treatment suppresses SIRT1 deacetylase activity, resulting in elevated p53 acetylation and activation, thereby triggering senescence.[64] Overexpression of platelet-derived growth factor (PDGF) receptor α in adult islets enhances β-cell proliferation and regeneration; however, PDGF expression gradually diminishes with aging.[65] Research suggests that APS promotes murine pancreatic β-cell proliferation by upregulating miR-6-136p and miR-5-149p while suppressing EFHD5 expression.[66] Concurrently, the antioxidant effects of AS-IV mitigate OS-induced β-cell damage. Huangqi (Astragali Radix)-mediated stimulation of β-cell regeneration may compensate for age- and apoptosis-related cell loss, thereby preserving islet functional stability. Currently, studies on the anti-senescence effects of Huangqi (Astragali Radix) remain limited, which warrants further experimental exploration to elucidate its mechanisms and therapeutic potential.

 

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Summary

Current research demonstrates that Huangqi (Astragali Radix) and its active components exhibit beneficial effects in mitigating glucolipotoxicity, reducing pancreatic β-cell death, modulating dedifferentiation and transdifferentiation, regulating immunity, and delaying cellular senescence. However, several limitations persist in existing studies: (1) mechanistic complexity: although components like APS and AS-IV act through multiple signaling pathways, the diverse constituents of Huangqi (Astragali Radix) may interact synergistically or antagonistically, and their precise molecular mechanisms remain incompletely elucidated. (2) Discrepancies between in vitro and in vivo studies: most research is confined to animal models and cell experiments, with a scarcity of randomized controlled trials to validate efficacy and safety in humans. (3) Standardization and dosage challenges: variations in geographical origin, processing methods, and extraction techniques lead to inconsistent bioactive compound profiles and pharmacological activities. Moreover, standardized preparation protocols and optimized dosing regimens are lacking. (4) Insufficient investigation of combination therapies: while combination therapy is common in clinical DM management, studies on Huangqi (Astragali Radix)'s interactions with conventional hypoglycemic agents—whether synergistic or adverse—remain limited. Future research should prioritize: (1) mechanistic exploration: leveraging single-cell sequencing and CRISPR-Cas9 gene editing to systematically dissect Huangqi (Astragali Radix)'s molecular networks in β-cell regeneration, transdifferentiation, and immune microenvironment modulation, clarifying cross-pathway interactions. (2) Advancing clinical research: conducting multicenter, large-scale clinical trials to evaluate Huangqi (Astragali Radix)'s therapeutic efficacy and safety in humans, alongside establishing precision medicine approaches and quality control standards. (3) Combination therapy optimization: systematically assess Huangqi (Astragali Radix)'s interactions with existing antidiabetic drugs to identify optimal combinatorial strategies for enhanced DM treatment outcomes. In conclusion, Huangqi (Astragali Radix) holds promising potential for broader recognition and application in DM therapeutics.

 

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Conflict of Interest

The authors declare no conflict of interest.

CRediT Authorship Contribution Statement

Liyi Yan: Investigation, and writing-original draft. Zhenhua Li: Supervision, and writing-review & editing. Yuan Chen: Conceptualization, funding acquisition, and writing-review & editing.

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Publication History

Received: 02 January 2025

Accepted: 28 February 2025

Article published online:
27 June 2025