Medicinal Plant Research 2025, Vol.15, No.3, 129-141 http://hortherbpublisher.com/index.php/mpr 130 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).
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