1 Introduction

Ginsenosides, belonging to damane triterpene saponins, are characterized by a steroid-like tetracyclic skeleton and multiple glycosides linked at specific sites (Kim et al., 2017; Im, 2020). According to the position of the sugar residue, ginsenosides are mainly classified into the protoginsenodiol type (PPD), and the protoginsenotriol type (PPT). PPD (e.g., Rb1, Rb2, Rc, Rd, Rg3) contain sugar groups at the C-3 site, while PPT-type (like Rg1, Re, Rf, Rg2) contain sugar groups at the C-6 site (Kim et al., 2017; Im, 2020; Jang et al., 2023). This structural diversity determines the extensive biological activities, exhibited by different ginsenosides.

Among the nearly 100 identified ginsenosides, Rg1, Rb1 and Rg3 are the most widely studied representative components, for their anti-inflammatory effects (Gao et al., 2020a; Im, 2020; Wang et al., 2022; Qu et al., 2025). Rg1 and Rb1 are abundant in Asian ginseng and American ginseng, while Rg3 is mainly enriched in processed (red ginseng) ginseng, and is renowned for its significant anti-inflammatory and antioxidant activities (Gao et al., 2020a; Wang et al., 2022; Qu et al., 2025). Other important ginsenosides with potential anti-inflammatory effects include Rc, Rd, Re, Rh1 and compound K (Yi, 2019; 2021; Jang et al., 2023).

Inflammation is a complex multi-step immune response of the body to infection or injury, involving the activation of innate immune cells, and the release of pro-inflammatory mediators (Kim et al., 2017; Gao et al., 2020b; Jang et al., 2023). The key signaling pathways involved in the inflammatory cascade response include nuclear factor κB (NF-κB), mitogen-activated protein kinase (MAPKs), Janus kinase-signal transducer and activator of transcription (JAK-STAT), and phosphatidylinositol 3-kinase-Akt (PI3K-Akt) (Gao et al., 2020a; b; Yi, 2021; Wang et al., 2022; Qu et al., 2025). These pathways regulate the expression of cytokines (TNF-α, IL-1β, IL-6 etc.) and related enzymes (such as iNOS, COX-2), thereby driving the inflammatory response (Kim et al., 2017; Wang et al., 2022; Jang et al., 2023).

Chronic and unresolved inflammation, is an important factor in the occurrence and development of various diseases, including metabolic diseases, cardiovascular diseases, neurodegenerative diseases and malignant tumors, etc. (Im, 2020; Wang et al., 2022). The continuous activation of inflammatory signaling pathways can lead to tissue damage, immune dysregulation and pathological occurrence of diseases (Im, 2020).

Ginseng has been used in traditional medicine for a long time, but the exact molecular mechanism by which ginsenosides exert anti-inflammatory effects has not been fully elucidated. This study attempts to reveal the pharmacological mechanism of ginsenosides, with a focus on their regulation of inflammatory signaling pathways, cytokine production, and immune cell function. A thorough understanding of the anti-inflammatory mechanism of ginsenosides will provide a theoretical basis for the development of new anti-inflammatory therapeutic drugs based on ginsenosides. This type of drug, is expected to become a safer and more effective alternative to existing anti-inflammatory drugs, and has broad application prospects in the prevention and treatment of various inflammation-related diseases.

2 Pharmacological Basis of Ginsenosides

2.1 Structural features and classification

Ginsenosides, are the main active saponins in plants of the genus Panax (Panax ginseng and related species), and are classified into two types according to their structure: PPD and PPT. The characteristic of PPD-type ginsenosides (Rb1, Rb2, Rc, Rd, Rg3, CK) is that a glycogroup is attached at the C-3 site of the damane skeleton, while PPT-type ginsenosides (Rg1, Re, Rf, Rg2, Rh1), are attached at the C-6 site (Mohanan et al., 2018; Zhang et al., 2024). This structural difference affects its pharmacological activity. The PPD type shows stronger anti-inflammatory and anti-cancer effects, while the PPT type plays a role in neuroprotection and cardiovascular protection (Ratan et al., 2021; Zhang et al., 2024).

Rare ginsenosides, like Rg3, Rh2 and compound K (CK), have a low content in nature, but can be generated through processing (steaming) or metabolic transformation by intestinal flora (Sharma and Lee, 2020; Fan et al., 2024). These rare saponins have stronger biological activity and better pharmacokinetic properties, and exhibit better anti-inflammatory, immunomodulatory and anticancer effects, compared with their parent compounds (Fan et al., 2024). Structure-activity relationship studies have shown that, deglycosylation (removal of glycogroups) can increase the lipophilicity and membrane permeability of molecules, thereby enhancing their biological efficacy (Li et al., 2024).

2.2 Pharmacokinetics and in vivo metabolism

Due to its large molecular weight, poor membrane permeability and easy degradation in the gastrointestinal tract, the oral bioavailability of ginsenosides is relatively low (Won et al., 2019; Jeon et al., 2021). Among the main types, the oral bioavailability of PPT-type ginsenosides, like Rg1 and Re, is generally better than that of PPD-type ones (such as Rb1, Rb2), which may be related to the differences in metabolic stability and absorption rate (Won et al., 2019). Rare ginsenosides and their metabolites (CK), exhibit better absorption and in vivo exposure levels (Sharma and Lee, 2020).

After oral administration, ginsenosides undergo extensive metabolic transformation, mainly under the action of liver and intestinal microbiota (Jeon et al., 2021; Park, 2024). The gut microbiota plays a role in the deglycosylation process of major ginsenosides, and can convert them into more active and easily absorbed forms, such as CK and Rh3 (Jeon et al., 2021; Park, 2024). These metabolites exhibit stronger anti-inflammatory and antioxidant effects than the parent compounds, highlighting the importance of biotransformation in mediating the in vivo effects of ginsenosides (Sharma and Lee, 2020; Jeon et al., 2021).

2.3 Overview of pharmacological effects

Ginsenosides, promote the resolution of inflammation by inhibiting pro-inflammatory cytokines (e.g., TNF-α, IL-1β, and IL-6), suppressing key inflammatory signaling pathways, like NF-κB, MAPKs, and JAK-STAT, and by promoting the polarization of M2-type macrophages. Thereby exerting anti-inflammatory effects (Mohanan et al., 2018; Li et al., 2022; Wang et al., 2022; Zhang et al., 2024). Ginsenosides also have strong antioxidant activity, and can reduce oxidative stress and protect tissues from damage, by regulating pathways such as Nrf2/HO-1 and PI3K/Akt (Hyun et al., 2022). Meanwhile, they can also enhance immunomodulatory functions, expand their broad therapeutic potential (Mohanan et al., 2018; Im, 2020; Fan et al., 2024).

Ginsenosides also have neuroprotective effects, which can relieve neuroinflammation, reduce oxidative damage, and inhibit neuronal apoptosis (Cheng et al., 2019; Jiang et al., 2025). In terms of the cardiovascular protection of ginsenosides, their functions include preventing ischemia-reperfusion injury, improving vascular function and regulating lipid metabolism (Fan et al., 2020; Ratan et al., 2021). These effects are mediated through multiple signaling pathways, like AMPK, Nrf2 and TGF-β, further demonstrating the pleiotropy of ginsenosides (Ratan et al., 2021).

3 Ginsenoside-Mediated Regulation of Inflammatory Signaling Pathways

3.1 Inhibition of NF-κB signaling

Ginsenosides, containing Rb1, Rb3, Rh1 and compound K, have been widely proven to inhibit the activation of the NF-κB pathway, which is a core regulatory factor of inflammation. One of its main mechanisms is to stabilize the IκB protein, retaining NF-κB in the cytoplasm, and preventing it from entering the nucleus. Ginsenosides can inhibit the phosphorylation and subsequent degradation of IκBα, maintain its inhibitory effect on NF-κB, and thereby block the transcription of pro-inflammatory genes (Kim et al., 2017; Lee et al., 2022; Jang et al., 2023). This effect has been validated in various cell types, including macrophages, endothelial cells and epithelial cells, and is closely associated with weakened inflammatory responses in in vivo, and in vitro models (Lu et al., 2019; Gao et al., 2020a; Nam et al., 2024).

By stabilizing IκB and inhibiting the activation of NF-κB, ginsenosides can down-regulate the expression of a series of pro-inflammatory genes. Including cytokines (TNF-α, IL-1β, IL-6), chemokines, adhesion molecules (VCAM-1, ICAM-1), and related enzymes (iNOS, COX-2) (Gao et al., 2020a; Jang et al., 2023). This broad inhibition of inflammatory mediators is an important mechanism, by which ginsenosides exert anti-inflammatory effects in acute and chronic inflammatory models, such as colitis, lung injury and vascular inflammation (Hsieh et al., 2018; Lu et al., 2019).

3.2 Modulation of MAPK signaling

Ginsenosides can also regulate the mitogen-activated protein kinase (MAPK) signaling pathway, which includes p38, ERK and JNK. These kinases play a role in inflammatory signaling, and the activation of transcription factors (AP-1 and NF-κB). Studies have shown that, ginsenosides such as Rb1, Rb3, Rd, Rg1 and Rh1, can inhibit the phosphorylation and activation of p38 and JNK under inflammatory stimulation, but have a relatively weak inhibitory effect on ERK (Huynh et al., 2020; Xu et al., 2022; Jin et al., 2023; Nam et al., 2024).

By inhibiting the MAPK signaling pathway, ginsenosides reduced the transcription of inflammation-related genes, including those encoding cytokines, chemokines, and matrix metalloproteinases (MMPs) (Kim et al., 2017; Gao et al., 2020a; Arafa et al., 2021). This effect has been verified in various inflammatory models, such as lung injury, periodontitis and colitis, and contributes to the overall anti-inflammatory, and tissue-protective effects of ginsenosides (Lu et al., 2019; Sun et al., 2020).

3.3 Roles of JAK/STAT and Nrf2 pathways

Some small molecule ginsenosides (Rg2, Rh1, Rk1, Rh4 etc.), have been proven to inhibit the JAK/STAT pathway, especially the phosphorylation of STAT1 and STAT3, which play a role in pro-inflammatory cytokine transcription (Huynh et al., 2020; Jin et al., 2022; To et al., 2022). By blocking the activation of JAK/STAT, ginsenosides reduced the expression of cytokines and inflammatory mediators in macrophages, endothelial cells and other immune cells, alleviating local and systemic inflammation (Huynh et al., 2020).

Ginsenosides can also activate the Nrf2 pathway, which is a core regulatory factor in antioxidant and cellular protective responses. Ginsenosides, liek Rg1, Rh2, Rb1, can promote the nuclear translocation of Nrf2, thereby up-regulating genes driven by antioxidant response elements (ARE), such as HO-1, SOD and catalase (Hsieh et al., 2018; Li et al., 2023; Zhou et al., 2025) (Figure 1). This not only enhances the antioxidant defense ability of cells, but inhibits the expression of pro-inflammatory genes by reducing oxidative stress (Li et al., 2023; Zhou et al., 2025). The dual role of Nrf2 in the antioxidant and anti-inflammatory processes, is one of the important mechanisms by which ginsenosides show therapeutic potential in chronic inflammatory diseases (Li et al., 2023; Zhou et al., 2025).

Figure 1 Effects of GS-Rg1 on inflammatory injury of periodontal tissue. (A) Chemical structure of GS-Rg1. (B) Inflammatory cell counts of the groups (n). (C) H&E staining was used to detect the periodontal histopathological changes. M1 = first molar; C = cementum; AB = alveolar bone; GE = gingival epithelium; and PL = periodontal ligament. (D)–(F) Representative images of Immunohistochemistry (IHC) detected the expression of IL-6 and TGF-β1 and statistical analysis of positive area. (G) and (I) qPCR quantification of the mRNA levels of IL-6 and TGF-β1 in different groups. * P < 0.05, reference Ctrl; # P < 0.05, reference PD; & P < 0.05, reference GS-Rg1 (Adopted from Zhou et al., 2025) Image caption: After Rg1 treatment, the number of inflammatory cells was markedly reduced, and epithelial integrity was restored. Immunohistochemistry and qPCR results further showed that IL-6 levels were significantly elevated and TGF-β1 was decreased in the model group, whereas the Rg1 group reversed this trend. Overall, the findings reveal that Rg1 can effectively alleviate local inflammatory responses and improve pathological damage in periodontal tissues (Adopted from Zhou et al., 2025)

4 Immunomodulatory Effects of Ginsenosides

4.1 Regulation of innate immunity

Ginsenosides exert their functions by regulating the activation state of innate immune cells, especially macrophages, and the secretion of cytokines. Whether it is PPD or PPT-type ginsenosides, they can promote or inhibit the activity of macrophages, according to different environments and concentrations (You et al., 2022; Paik et al., 2023; Qian et al., 2024; Zhang et al., 2024). For instance, Rg1 and Rg3 can promote the polarization of macrophages to the anti-inflammatory M2 type, reduce the production of pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6, and increase the levels of anti-inflammatory factors IL-10 (Paik et al., 2023; Qian et al., 2024). Ginsenosides can also inhibit the activation of inflammasomes (NLRP3), further reducing the inflammatory response (Zhao et al., 2024). Under the action of ginsenosides, the phagocytic activity of macrophages and the production of reactive oxygen species (ROS) are enhanced, which is conducive to pathogen clearance (Yang et al., 2018).

Ginsenosides, especially Rg1, have also been shown to promote the maturation of dendritic cells (DCs), manifested as increased expression of surface markers, like CD86, and enhanced secretion of IL-12 and TNF-α (Qu et al., 2011). Mature DCs can enhance antigen presentation and T cell activation ability (Tang et al., 2024; Zhang et al., 2024). In vivo experiments, Rg1 can increase the number of DCs, and enhance their ability to stimulate T and B lymphocytes, thereby playing a role between innate immunity and adaptive immunity (Tang et al., 2024).

4.2 Influence on adaptive immunity

Ginsenosides affect the immune response of T helper cells (Th), by regulating the differentiation of T cell subsets. For instance, Rg1 can promote Th2 differentiation, enhance IL-4 production, and simultaneously inhibit Th1 response (IFN-γ), thereby improving the pathological state characterized by Th1 dominance (You et al., 2022). Other ginsenosides, like Rd and Rg3, can simultaneously enhance the production of Th1 and Th2 cytokines and maintain the balance of the immune response (Guo et al., 2022).

Under the action of ginsenosides, the humoral immune function is also enhanced. Studies have shown that, Rg1, Rg2 and Re can promote B cell proliferation and antibody production, increase the levels of IgG, IgA and IgM in animal models, and act as adjuvants to enhance the antibody response induced by vaccines (You et al., 2022; Guo et al., 2022; Tang et al., 2024). This effect is partially achieved by activating T follicular helper cells (Tfh), and promoting cytokines that support B cell differentiation and function (Dong et al., 2017; Guo et al., 2022).

4.3 Cross-regulation of inflammation and immunity

Ginsenosides exhibit dual immunomodulatory effects, and can act as either immunostimulants or immunosuppressants depending on the immune environment (You et al., 2022; Zhang et al., 2024). For instance, Rg1 and CK can enhance immune tolerance, while suppressing excessive inflammatory responses. The mechanisms include promoting Treg differentiation, and inhibiting Th17-mediated inflammation (Dong et al., 2017).

Ginsenosides finely regulate immune responses by regulating a wide range of signaling pathways, including NF-κB, MAPK, PI3K/Akt and STAT (Cheng et al., 2019; Tang et al., 2024; Zhang et al., 2024). They can down-regulate pro-inflammatory cytokines (TNF-α, IL-1β, IL-6 etc.), and up-regulate anti-inflammatory mediators (such as IL-10), thereby contributing to the resolution of inflammation and the restoration of immune homeostasis (You et al., 2022; Paik et al., 2023; Zhang et al., 2024).

5 Cellular and Molecular Evidence of Anti-inflammatory Mechanisms

5.1 Cell-based studies

A large number of studies using LPS-stimulated macrophage models, especially RAW264.7 cells and bone marrow-derived macrophages, have clarified the anti-inflammatory effects of ginsenosides. Studies have shown that ginsenosides, such as Rb1, Rg1, Rg3, Rh2, Rh4, compound K and Rc, can inhibit pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in these models. And the production of inflammatory mediators (iNOS, COX-2, NO, PGE2) (Gao et al., 2020a; To et al., 2022; Qu et al., 2025). Mechanically, these effects are associated with the inhibition of key signaling pathways, including TLR4/NF-κB, MAPKs (p38, JNK, ERK), and STAT3, and involve direct interference with TLR4 dimerization and inflammasome activation (To et al., 2022; Xu et al., 2022).

In the ginsenoside treated cell model, the expression and secretion of inflammatory mediators, including NO, PGE2 and ROS, decreased, while the expression of co-stimulatory molecules and adhesion factors was downregulated (Im, 2020; To et al., 2022; Bruggink et al., 2025). These changes were confirmed at both mRNA and protein levels, and were often detected by qPCR, ELISA and Western blotting, accompanied by decreased activities of transcription factors such as NF-κB and AP-1 (Lee et al., 2022; Kang et al., 2023). Some studies have also reported that, the regulation of lipid mediator profiles and their inhibitory effects on inflammasome components (NLRP3, caspase-1) (Yi, 2019; Shi et al., 2020; To et al., 2022).

5.2 Animal model studies

The anti-inflammatory efficacy of ginsenosides has been verified in various animal models, including acute kidney injury induced by LPS or cantharidin, septic shock, ear swelling, colitis induced by DSS or TNBS, and acute lung injury, etc. (Chen et al., 2021; Long et al., 2022; Xu et al., 2022). Studies have shown that ginsenosides, like Rb1, Rg1, Rg3, Rh2, Rc and compound K, can continuously reduce the severity of diseases, tissue damage and mortality. Meanwhile, in the colitis model, they can also improve clinical indicators such as body weight, colon length and disease activity index (Qu et al., 2025) (Figure 2).

Figure 2 Supplementation with Rg1, Rg3, and Rf blunted DSS-induced colitis. (A) Schematic diagram for the establishment of colitis mice model with Rg1, Rg3, and Rf. Effect of Rg1, Rg3, and Rf on (B) body weight, (C) DAI scores, (D) colon lengths, and (E) coefficient of the spleen in DSS-induced mice (n = 6). (F) Representative pictures of H&E stained histological sections of the colon in mice. Scale bars = 200 µm. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with the blank group; # p < 0.05 and ## p < 0.01 compared with the DSS group (Adopted from Qu et al., 2025)

Histopathological analysis indicated that, ginsenoside treatment could reduce inflammatory cell infiltration, tissue edema and organ structure damage (Hsieh et al., 2018; Yang et al., 2018; Gao et al., 2020a; Xu et al., 2022). Serum and tissue tests showed that, the levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) decreased, while the level of anti-inflammatory cytokine (IL-10) increased, further supporting the systemic anti-inflammatory effect of ginsenosides (Gao et al., 2020b; Chen et al., 2021; Long et al., 2022).

5.3 Molecular target validation

Western blotting and immunofluorescence techniques, are widely used to validate the molecular targets of ginsenosides in cell and animal models. These experiments confirmed the inhibitory effect on key inflammatory signaling proteins (e.g., NF-κB p65, STAT3, p38 MAPK), as well as the down-regulation of inflammatory mediators at the protein level (Gao et al., 2020a; Kang et al., 2023; Nam et al., 2024). Immunofluorescence experiments further demonstrated the nuclear translocation of transcription factors, like NF-κB decreased, mechanologically supporting the basis of ginsenoside action (Lee et al., 2022; Nam et al., 2024; Pan et al., 2024).

Studies on gene knockout and overexpression, have provided direct evidence for the involvement of specific molecular targets in the anti-inflammatory effects of ginsenosides. For instance, studies using TLR4, STAT3 or MerTK deletion models have shown that, the anti-inflammatory effect of ginsenosides depends on these pathways (Yang et al., 2018; Gao et al., 2020; To et al., 2022). The overexpression of TLR4 or STAT3, can partially reverse the inhibitory effect of ginsenosides on inflammatory signals, further confirming their direct molecular targets (Xu et al., 2022).

6 Clinical Applications and Anti-inflammatory Potential

6.1 Clinical trials and progress

The therapeutic potential of ginsenosides in a variety of chronic inflammatory diseases has been explored, including colitis, rheumatoid arthritis, chronic sinusitis and inflammatory lung disease. Preclinical studies and limited clinical trials have shown that ginsenosides such as Rg1, Rg3, Rb1, Rh2 and compound K can alleviate disease severity, tissue inflammation and clinical symptoms in models of colitis, arthritis and lung injury (Gao et al., 2020a; Kim et al., 2021; Zhang et al., 2021; Wang et al., 2022). For instance, Rg1 performs exceptionally well in alleviating colitis, and its mechanism is related to regulating macrophage polarization and restoring the intestinal metabolite profile (Qu et al., 2025). Rg3 has been proven to have therapeutic effects in reducing pulmonary inflammation, neuroinflammation and organ damage, and this effect has been supported in both animal experiments and early clinical trials (Wang et al., 2022).

Regarding the safety of ginsenosides, most studies have shown that they have very few adverse reactions at therapeutic doses (Gao et al., 2020b; He et al., 2020; Jang et al., 2023). In animal experiments and early human trials, ginsenosides did not show obvious toxicity or organ damage. The efficacy of some preparations could even be comparable to that of commonly used non-steroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids, but with fewer side effects (Lee et al., 2018; 2019; He et al., 2020). But, large-scale, well-designed clinical trials are still limited, and their long-term safety and efficacy require further studies to be fully validated in different patient populations (Kim et al., 2017; Jang et al., 2023).

6.2 Comparison with conventional anti-inflammatory drugs

Ginsenosides exert their effects through multi-target mechanisms, including inhibiting NF-κB, MAPK and JAK/STAT pathways, and regulating immune cell function and cytokine expression (Im, 2020; Yi, 2021; To et al., 2022; Wang et al., 2022). Unlike traditional NSAIDs and glucocorticoids, these drugs take effect through a single pathway and often cause immunosuppression or metabolic side effects. Ginsenosides can not only inhibit excessive inflammation, but promote the resolution of inflammation by promoting the polarization of M2-type macrophages, and exerting antioxidant effects (Yang et al., 2018; Lee et al., 2022; Jang et al., 2023). Some studies suggest that, ginsenosides can be used in combination with conventional drugs to improve efficacy, and reduce the required dose, thereby potentially reducing the risk of adverse reactions (He et al., 2020; Arafa et al., 2021).

One key advantage of ginsenosides over traditional anti-inflammatory drugs is their lower risk of adverse reactions. For instance, Rg1 can act as a selective glucocorticoid receptor agonist, exerting anti-inflammatory effects without damaging tissue regeneration, while impaired tissue repair is a common side effect of glucocorticoids (He et al., 2020). Black ginseng exhibited anti-inflammatory efficacy comparable to that of NSAIDs due to the change in saponin profile, but with better safety (Lee et al., 2019).

6.3 Development of functional foods and health products

The research and development as well as commercialization of functional foods and nutritional health products based on ginsenosides are advancing rapidly. To maximize anti-inflammatory efficacy and bioavailability, researchers developed ginsenoside-enriched extracts such as AP-SF and rare ginsenosides of ginseng fruit (GFRS) (Zheng et al., 2024). Microbial and enzymatic conversion techniques are being applied to convert major ginsenosides into secondary ginsenosides, with stronger pharmacological activity, such as compound K and gynostemma pentaphyllum saponin XVII, which exhibit better anti-inflammatory activity (Zhou et al., 2023).

Ginsenoside dietary supplements are increasingly being promoted for the prevention and management of inflammation-related diseases. Clinical and preclinical studies support its application in reducing inflammatory markers, improving intestinal health and alleviating symptoms of chronic diseases (Qu et al., 2025). Its safety and efficacy have been generally supported by animal and early human trials, but regulatory approval and standardization remain current challenges (Zheng et al., 2024; Niu et al., 2025).

7 Case Studies

7.1 Anti-inflammatory mechanisms of ginsenoside Rb1

Ginsenoside Rb1, plays a prominent role in the protection against cardiovascular inflammation. It can exert its effects by reducing the expression of pro-inflammatory cytokines and inhibiting the infiltration of inflammatory cells in vascular tissues. Rb1 can regulate the dimerization of Toll-like receptor 4 (TLR4), thereby weakening downstream inflammatory signals in cardiovascular and renal models (Gao et al., 2020a; Im, 2020). In animal studies, Rb1 can alleviate acute kidney injury and reduce mortality in sepsis models, highlighting its systemic anti-inflammatory potential (Gao et al., 2020a).

The anti-inflammatory mechanism of Rb1 is closely related to its inhibition of the NF-κB pathway. It inhibits the activation of NF-κB and MAPK by preventing TLR4 dimerization, reducing the recruitment of MyD88 and the expression of TAK1 (Gao et al., 2020a). This process leads to a reduction in the production of inflammatory mediators such as TNF-α, IL-1β, iNOS and COX-2, which has been verified in both in vivo and in vitro models (Gao et al., 2020a; Im, 2020).

7.2 Applications of rare ginsenosides Rg3

Rare ginsenoside Rg3, exhibits potent anti-inflammatory effects in cancer-related environments. Rg3 can inhibit the activation of NLRP3 inflammasome, suppress NF-κB signaling, and reduce the secretion of pro-inflammatory cytokines in the tumor microenvironment (Im, 2020; Shi et al., 2020; Wang et al., 2022). Rg3 can also promote the polarization of M2-type macrophages, contribute to the resolution of inflammation, and may regulate tumor progression (Yang et al., 2018; Im, 2020).

Rg3 has shown therapeutic effects in various inflammatory disease models, including acute lung injury, neuroinflammation and asthma. Its effects are manifested in reducing tissue damage, lowering inflammatory cell infiltration and inhibiting cytokine production (Yang et al., 2018; Wang et al., 2022). Its multi-target and multi-pathway mechanisms - such as activating the PI3K/AKT/mTOR pathway, and inhibiting NF-κB - further support its potential as a treatment for chronic inflammation and oxidative stress-related diseases (Wang et al., 2022) (Figure 3). Rg3 has demonstrated anti-inflammatory effects in both preclinical and early clinical studies, highlighting its promising application prospects in future drug development.

Figure 3 Functional mechanisms and targets of Rg3 on antioxidant and anti-inflammatory effects. Rg3 upregulates Nrf2 to enhance antioxidase activity. Rg3 inhibits the NF-κB pathway and downstream COX-2 to ameliorate inflammation and oxidative stress. Rg3 activates SIRT1 to inhibit the NF-κB pathway. Rg3 protects tissue from apoptosis through the PI3K/Akt pathway (Adopted from Wang et al., 2022)

8 Conclusions and Perspectives

Ginsenosides are the most important active components in ginseng. Their anti-inflammatory effect is mainly achieved by inhibiting the expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and inflammation-related enzymes (iNOS, COX-2). These effects involve the regulation of pathways, such as NF-κB, MAPK, JAK/STAT, and PI3K/Akt. Meanwhile, ginsenosides can also promote the polarization of macrophages and microglia towards M2 type, which helps to reduce inflammation and maintain tissue homeostasis.

There are also differences among different saponin molecules. Rg3 has attracted attention due to its multi-target and multi-pathway characteristics and has performed outstandingly in lung, liver and neuroinflammatory models. Research on Rb1, Rg1 and Rh2 has been relatively in-depth, mainly focusing on inhibiting inflammatory mediators and regulating immune responses. Some secondary saponins and their derivatives (like compounds K, Rh4), exhibit stronger anti-inflammatory efficacy and even present new mechanisms of action.

But, most of the current evidence comes from cell and animal experiments, and clinical research is still significantly insufficient. There is a lack of large-scale, strictly designed trials to verify its efficacy and safety in the population. Clinical transformation still faces many challenges, such as differences in ginsenoside content, individual differences among patients, and the gap in formulation standardization. Besides, its low oral utilization and rapid metabolism also increase the difficulty of dose optimization and application.

Future research will need to rely on multi-omics approaches, like genomics, proteomics and metabolomics, to more systematically reveal the mechanism of action of ginsenosides and search for new therapeutic targets. In the field of medicinal chemistry, through molecular modification or enzymatic transformation, some derivatives with stronger activity and better stability have been obtained. With the continuous development and clinical verification of new compounds, it is expected that safe and effective ginsenoside anti-inflammatory drugs will be formed, providing new options for the treatment of various inflammatory diseases.

Acknowledgments

The authors sincerely thank Dr. Wang for reviewing the manuscript and providing valuable suggestions, which contributed to its improvement. Additionally, heartfelt gratitude is extended to the two anonymous peer reviewers for their comprehensive evaluation of the manuscript.

Conflict of Interest Disclosure

The authors affirm that this research was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest.

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