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Tangs Vitigo are botanical compound comprises two formulas.

As early as the Sui dynasty, the Treatise on the Origins and Symptoms of Disease recorded that vitiligo arises when wind lodges in the skin and qi and blood lose their harmony. The Ming dynasty Orthodox Manual of External Medicine added that white patches specifically reflect stagnation of qi, with qi and blood congealed at the pores and failing to circulate. In the Qing dynasty, Correcting the Errors in the Forest of Medicine described blood stasis within the skin.

These formulas follow that line of reasoning: they work principally by moving blood and freeing the movement of qi, combined with dispersing wind and supporting the liver and kidney, so that qi and blood can once again reach the skin.

Diagnosis first: not every pale patch is vitiligo. Pityriasis versicolor, post-inflammatory hypopigmentation and pityriasis alba can all produce white patches, and are treated quite differently. If a patch has fine scale on its surface or is itchy, please have it assessed by a dermatologist first.

Recovery in vitiligo is typically slow and requires sustained treatment over an extended period. Your physician assesses the border, colour and stability of the patches together with your general condition. These are prescription formulas and require consultation and pattern diagnosis by a physician.

Indications

Psoriasis (Plaque Psoriasis, Guttate Psoriasis, Inverse Psoriasis, Pustular Psoriasis), Eczema (Atopic Dermatitis), Vitiligo

Not offered as first-line care: generalised pustular psoriasis and erythrodermic psoriasis are potentially life-threatening dermatological emergencies. Patients with these forms must be assessed by, and remain under the care of, a registered dermatologist. Tangs Vitigo is not offered as an alternative to emergency or specialist medical care.

Contraindications

Do Not Take Tangs Vitigo If You:

  • are pregnant
  • are taking warfarin or any other anticoagulant or antiplatelet medication — this formula contains Radix Salviae Miltiorrhizae (Danshen), Flos Carthami (safflower) and Radix Angelicae Sinensis, all of which may increase bleeding risk
  • have a known allergy to any ingredient listed below
  • have significant liver or kidney impairment, unless cleared by your doctor
  • are scheduled for surgery within two weeks

Do Not Take Together With:

Corticosteroids and other immunosuppressants, both conventional and herbal (including UVB and PUVA phototherapy). Full list: Corticosteroids or immunosuppressive drugs. (Herbal and Conventional)

Commonly overlooked items on that list include fish oil, flaxseed oil, evening primrose oil, turmeric, resveratrol, chia seeds, cordyceps, Centella asiatica and cassia seed. Please tell us everything you are taking, including supplements and health foods.

Stop and Seek Medical Attention If:

Unusual bruising, nosebleeds, or bleeding that does not stop; jaundice or dark urine; rapidly spreading redness over most of the body; difficulty breathing or facial swelling.

Prognosis of the Immunosuppressants Withdraw Syndrome:
波浪式反复(免疫抑制剂反弹症)

 

 

  • Tangs Vitigo is not given alongside corticosteroids or other immunosuppressants. Where a patient is already receiving such treatment, any change must be planned and supervised by the doctor who prescribed it. Systemic corticosteroids in particular must never be stopped abruptly: abrupt withdrawal can cause adrenal insufficiency, and can trigger a severe generalised flare of an underlying inflammatory skin disease. We will not begin herbal therapy until a withdrawal plan has been agreed with the prescribing doctor.
  • Patients with a history of immunosuppressant use, and in particular those treated for eczema or psoriasis, will likely start to experience the so-called Wavelike Flare-up Cycle (above figure). This is known as the Immunosuppressant Withdrawal Syndrome. Symptoms previously suppressed by immunotherapy will start to resurface after the immune system is no longer being curtailed, then subside in frequency and intensity in a wavelike pattern over time. The time to reach the endpoint will depend on the dosage and potency of the immunosuppressants formerly consumed. This pattern describes inflammatory skin disease; vitiligo follows a different course, in which depigmentation may continue to spread before it stabilises, and repigmentation, if it occurs, is typically slow.
  • These are individual observations recorded during clinic follow-up, not controlled outcome data, and they do not predict the course of any other patient. Vitiligo, eczema and psoriasis are currently regarded in modern medicine as chronic conditions for which no cure is established. We make no claim that Tangs Vitigo cures any of them or prevents relapse.

Dosage

3000mg to be taken two times daily

Precaution

  • During the course of Tangs Vitigo therapy, abstain from all immunosuppressants and oral contraceptive pills. Abstain from alcohol consumption and avoid late nights. Avoid hot baths, and do not aggravate the skin by scratching or peeling the psoriatic lesions. A more relaxed lifestyle is recommended.
  • Have a known allergy to any ingredient listed below／对下列任一成分已知过敏

Ingredients

Tangs Vitigo-1, each 360mg extract equivalent to 3212mg raw herbs:
Radix Salviae Miltiorrhizae [1-4] 250mg
Lignum Dalbergiae Odoriferae [5-9] 500mg
Flos Carthami [10-14] 625mg
Radix Saposhnikoviae [15-18] 333mg
Radix et Rhizoma Cynanchi Atrati [19,20] 125mg
Semen Cuscutae [21-23] 333mg
Radix Astragali [24-26] 255mg
Herba Moslae [27-29] 125mg
Radix Achyranthis Bidentatae [30-36] 333mg
Ramulus Cinnamomi [37-42] 333mg

Tangs Vitigo-2, each 360mg extract equivalent to 3115mg raw herbs:
Radix Angelicae Sinensis [43-50] 200mg
Radix Paeoniae Alba [51-57] 200mg
Radix Asparagi [58-61] 333mg
Radix Ophiopogonis [62-65] 333mg
Radix Salviae Miltiorrhizae [1-4] 250mg
Lignum Dalbergiae Odoriferae [5-9] 333mg
Flos Carthami [10-14] 600mg
Radix Saposhnikoviae [15-18] 333mg
Radix et Rhizoma Cynanchi Atrati [19,20] 200mg
Semen Cuscutae [21-23] 333mg

Clinical Evidence

Radix Salviae Miltiorrhizae [1-4]: tanshinones I and IIA suppress Th1 differentiation by inhibiting STAT3/STAT5 phosphorylation, reducing IFN-γ production [1]. Salvianolic acid A and tanshinone IIA decrease Th2 cytokines in allergic models [2]. Polysaccharides promote Treg differentiation and enhance CD8+ T cell cytotoxicity; those findings come from tumour-bearing mice and cancer patients [3,4] and are reported as mechanism only. The Th1/IFN-γ-suppressing activity is the direction consistent with current understanding of vitiligo; the CD8+-enhancing activity runs the other way and has not been reconciled.

Lignum Dalbergiae Odoriferae [5-9]: the evidence is in vitro and concerns suppression of pro-inflammatory mediators. Flavonoids and benzofurans from heartwood inhibit LPS-induced nitric oxide production in RAW264.7 macrophages, IC50 6.3–19.9 μM [5]; dalberavonoids A–C from the roots inhibit the same endpoint at IC50 9.13–12.58 μM versus 23.86 μM for indomethacin [6]. 4-Methoxydalbergione and 4′-hydroxy-4-methoxydalbergione promote Nrf2 nuclear translocation and induce heme oxygenase-1, suppressing iNOS and COX-2 in BV2 and primary rat microglia [7]. Latifolin suppresses NF-κB activation via Nrf2-mediated HO-1 induction, lowering nitrite, PGE2, TNF-α and IL-1β in peritoneal macrophages; tin protoporphyrin IX reverses this, confirming HO-1 as the mediating step [8]. Traditional use and phytochemistry are reviewed in [9].

Flos Carthami [10-14]: whole extract increases proliferation, migration and tube formation of human microvascular endothelial cells and enhances angiogenesis in zebrafish [10] — vascular activity consistent with the traditional role of this herb. The remaining evidence concerns hydroxysafflor yellow A (HSYA), the pharmacopoeial marker constituent. HSYA and kaempferol inhibit LPS-induced M1 macrophage activation, reducing TNF-α and IL-1β, and shift the M1/M2 balance [11]. In collagen-induced arthritis, HSYA reduced paw swelling, synovial pathology and serum cytokines by inhibiting ERK activation [12]. In sepsis, HSYA inhibited JAK2/STAT1 phosphorylation [13]; KEGG analysis in the same study additionally implicated Th17, IL-17, TNF, PI3K-Akt and NOD-like receptor pathways, but those are computational predictions. The JAK2/STAT1 result is the most directly relevant, since IFN-γ signalling through JAK and STAT1 is the axis targeted by the approved topical JAK inhibitor. Pointing the other way, HSYA enhanced recruitment and activation of tissue-resident memory T (TRM) cells in breast cancer models [14].

Radix Saposhnikoviae [15-18]: suppresses Th1 differentiation and function — reduced IFN-γ production and T-bet expression, decreased Th1/Th2 cytokine ratio — in murine allergic contact dermatitis, mediated in part by downregulation of dendritic cell maturation and costimulatory molecule expression [15]. Structural characterisation and further immunomodulatory data appear in [16-18]. The IFN-γ-suppressing direction is the one consistent with vitiligo pathogenesis.

Radix et Rhizoma Cynanchi Atrati [19,20]: suppresses iNOS and COX-2 by inhibiting IKK-mediated NF-κB signalling [19]. In a DNCB-induced murine model of atopic dermatitis it reduced IL-6, IL-1β, TNF-α and mast cell infiltration [20].

Semen Cuscutae [21-23]: Cuscuta chinensis seed extracts show antinociceptive and anti-inflammatory activity in mice [22] and protect osteoblastic cells against oxidative injury [23]. A topical nanoemulsion gel has been studied for wound healing [21].

Radix Astragali [24-26]: flavonoids suppress Th1 and Th17 differentiation and cytokine production (IFN-γ, IL-17) while promoting Treg differentiation, via JAK/STAT and NF-κB signalling [24,25] — the direction most relevant to vitiligo, since JAK/STAT inhibition is the mechanism of the topical JAK inhibitor approved for repigmentation. Other work reports the opposite: increased IL-4 and reduced IFN-γ indicating Th2 polarisation, with increased CD8 expression supporting cytotoxic T cell activation [26].

Herba Moslae [27-29]: the available evidence is respiratory and metabolic, not dermatological. Flavonoids attenuate influenza A virus-induced pulmonary endothelial barrier disruption by suppressing NOX4/NF-κB/MLCK signalling [27]; aqueous extract has been studied for antiviral activity in vitro [28]; and extract reduces uric acid and renal inflammation in a hyperuricemia model [29].

Radix Achyranthis Bidentatae [30-36]: the evidence points in two directions and neither was obtained in skin. In cyclophosphamide-immunosuppressed mice, Achyranthes bidentata polysaccharides raised IL-2, IL-6, IFN-γ and TNF-α and the CD3+CD4+ Th proportion, and at transcript level increased T-bet while decreasing GATA-3, Foxp3 and RORγt — a shift toward Th1 polarisation with reduced Treg-associated transcription [32]. They also induce dendritic cell maturation with increased MHC II, CD86, CD40 and IL-12 [33], enhance splenic lymphocyte proliferation when delivered in cubosome carriers [34], and selectively enhance Th1-mediated immunity in a malaria model [36]. Because vitiligo is driven by IFN-γ signalling and CD8+ T cells, and Treg activity is generally regarded as protective in it, this Th1-promoting, Foxp3-lowering profile is the opposite of the direction sought for that indication. Pointing the other way, in collagen-induced arthritis the polysaccharides reduced serum TNF-α by 37.1% and IL-6 by 42.3%, expanded short-chain-fatty-acid-producing Bacteroides and repaired intestinal barrier integrity [35]. Structure and bioactivity are reviewed in [30,31].

Ramulus Cinnamomi [37-42]: the evidence is anti-inflammatory in direction. Ramulus Cinnamomi essential oil, in which (E)-cinnamaldehyde is roughly 65% of content, inhibits N-acylethanolamine acid amidase, preventing degradation of PEA and OEA and reducing nitric oxide and TNF-α in LPS-stimulated macrophages [37]. In collagen-induced arthritis, Cinnamomi Ramulus extract reduced paw volume, arthritis index and TNF-α, IL-17A, IL-6 and IL-1β, implicating the TNF and IL-17 pathways and NF-κB p65 [38] — the IL-17 finding bears directly on the psoriasis indication of this formula. An ethanol extract blocks Src/Syk-mediated NF-κB activation in macrophages [39], and cinnamaldehyde suppresses macrophage cytokine output only in the presence of activated T cells, by eliminating reactive oxygen species [40].

Radix Angelicae Sinensis [43-50]: the effect depends on which polysaccharide fraction is studied, and the fractions act in opposite directions. Angelica sinensis polysaccharide promotes splenic T cell and macrophage proliferation, raises the CD4+ percentage and skews cytokines toward Th1 — upregulating IL-2 and IFN-γ while suppressing IL-4 [43]; structurally distinct fractions increase lymphocyte proliferation and IFN-γ, IL-2, IL-6 and TNF-α secretion [44]; and hydrosoluble fractions activate peritoneal macrophages through a TLR4-dependent, LPS-like mechanism [45]. Against this, a low-molecular-weight fraction (ASP-4, 23.18 kDa) is anti-inflammatory in the same cells, suppressing TNF-α, raising IL-10 and inhibiting iNOS, COX-2 and p65/IκB-α phosphorylation [46], so the same NF-κB pathway is engaged in opposite directions depending on structure. Delivered in PLGA nanoparticles the polysaccharide promotes dendritic cell maturation via JAK2/STAT3 [47]; that was a nanoparticle formulation, not the crude herb. Separately, the polysaccharide expands myeloid-derived suppressor cells and enhances their immunosuppressive function via STAT1/STAT3 [48] — immunosuppressive rather than stimulatory, and the one finding here that would dampen rather than amplify an autoreactive T-cell response, though it has not been examined in vitiligo. General pharmacology is reviewed in [49,50].

Radix Paeoniae Alba [51-57]: paeoniflorin and total glucosides of paeony act on NF-κB, MAPK, PI3K/Akt and JAK/STAT signalling [51-53]. In animal models of autoimmune disease — rheumatoid arthritis, experimental autoimmune encephalomyelitis and atopic dermatitis — these compounds reduce disease severity and inflammatory markers and promote immune tolerance by shifting Th1/Th2 activity [54,55]. Paeoniflorin delivered in hyaluronic acid hydrogel microspheres or as carbon dots in chitosan hydrogel accelerates wound closure and shifts macrophage polarisation from M1 to M2 [56,57].

Radix Asparagi [58-61]: both stimulates macrophage-mediated innate responses and suppresses pathological inflammation. Polysaccharides activate macrophages via TLR4-MAPK signalling, increasing TNF-α, IL-1β and IL-6 and promoting innate immune memory through histone modification [58,59]. Conversely, ethyl acetate extract suppresses nitric oxide, COX-2 and reactive oxygen species in activated macrophages [60], and methyl protodioscin inhibits cytokine production in airway inflammation [61].

Radix Ophiopogonis [62-65]: increases splenocyte proliferation, promotes the proportion of CD4+ and CD8+ T cells, and elevates cytokine production and antigen-specific antibody titres [62,63]. Liposomal polysaccharide formulations activate macrophages, increasing phagocytic activity, nitric oxide production and CD14 and MHC-II expression, and upregulating IL-1β and TNF-α through TLR4-NF-κB signalling and miR-4796 [64,65].

Reference

  1. Tang J, Zhao X. Research Progress on Regulation of Immune Response by Tanshinones and Salvianolic Acids of Danshen (Salvia Miltiorrhiza Bunge). Molecules. 2024;29(6):1201.
  2. Heo JY, Im DS. Anti-Allergic Effects of Salvianolic Acid A and Tanshinone IIA From Salvia Miltiorrhiza Determined Using in Vivo and in Vitro Experiments. Int Immunopharmacol. 2019;67:69-77.
  3. Ji H, Fan Y, Long Y, et al. Structural Analysis of Salvia Miltiorrhiza Polysaccharide and Its Regulatory Functions on T Cells Subsets in Tumor-Bearing Mice Combined With Thymopentin. Int J Biol Macromol. 2024;277(Pt 1):133832.
  4. Chen Y, Li H, Li M, et al. Salvia Miltiorrhiza Polysaccharide Activates T Lymphocytes of Cancer Patients Through Activation of TLRs Mediated-MAPK and -NF-κB Signaling Pathways. J Ethnopharmacol. 2017;200:165-173.
  5. Xu W, Zhu Q, Wang M, et al. (±)-Odoriferols A–E, Five Pairs of Enantiomeric Flavonoids and Benzofurans From Dalbergia Odorifera With Anti-Inflammatory Activity. Phytochemistry. 2026.
  6. Wu WY, Chen HJ, Cheng HL, et al. Three Novel Flavonoid Derivatives From the Roots of Dalbergia Odorifera. Chem Biodivers. 2025.
  7. Kim DC, Lee DS, Ko W, et al. Heme Oxygenase-1-Inducing Activity of 4-Methoxydalbergione and 4′-Hydroxy-4-Methoxydalbergione From Dalbergia Odorifera and Their Anti-Inflammatory and Cytoprotective Effects in Murine Hippocampal and BV2 Microglial Cell Line and Primary Rat Microglial Cells. Neurotox Res. 2018.
  8. Lee DS, Kim KS, Ko W, et al. The Neoflavonoid Latifolin Isolated From MeOH Extract of Dalbergia odorifera Attenuates Inflammatory Responses by Inhibiting NF-κB Activation via Nrf2-Mediated Heme Oxygenase-1 Expression. Phytother Res. 2014.
  9. Zhao X, Wang C, Meng H, et al. Dalbergia Odorifera: A Review of Its Traditional Uses, Phytochemistry, Pharmacology, and Quality Control. J Ethnopharmacol. 2020.
  10. Zhou X, Siu WS, Fung CH, et al. Pro-Angiogenic Effects of Carthami Flos Whole Extract in Human Microvascular Endothelial Cells in Vitro and in Zebrafish in Vivo. Phytomedicine. 2014;21(11):1256-63.
  11. Li Y, Zheng D, Shen D, et al. Protective Effects of Two Safflower Derived Compounds, Kaempferol and Hydroxysafflor Yellow A, on Hyperglycaemic Stress-Induced Podocyte Apoptosis via Modulating of Macrophage M1/M2 Polarization. J Immunol Res. 2020.
  12. Li DW, Wang XT, Mu BC, Dou DQ, Kang TG. Effects of Hydroxysafflor Yellow A on Rats With Collagen-Induced Arthritis. Biochem Biophys Res Commun. 2021.
  13. Pan B, Chen F, Shen S, et al. Hydroxysafflor Yellow A Modulation of Metabolite Networks and Inhibition of JAK2/STAT1 Pathway in Sepsis. Sci Rep. 2025.
  14. Zhou L, Lai G, Han B, et al. Hydroxy-Safflower Yellow A Inhibits Breast Cancer Growth via Tumor-Associated Macrophages/CCL5/Tissue Resident Memory T Cell Signaling. BioFactors. 2026.
  15. Yu X, Niu Y, Zheng J, et al. Radix Saposhnikovia Extract Suppresses Mouse Allergic Contact Dermatitis by Regulating Dendritic-Cell-Activated Th1 Cells. Phytomedicine. 2015;22(13):1150-8.
  16. Rao Z, Zhou H, Li Q, Zeng N, Wang Q. Extraction, Purification, Structural Characteristics and Biological Properties of the Polysaccharides From Radix Saposhnikoviae: A Review. J Ethnopharmacol. 2024;318(Pt A):116956.
  17. Fan H, Sun M, Li J, et al. Structure Characterization and Immunomodulatory Activity of a Polysaccharide From Saposhnikoviae Radix. Int J Biol Macromol. 2023;233:123502.
  18. He X, Fan H, Sun M, et al. Chemical Structure and Immunomodulatory Activity of a Polysaccharide From Saposhnikoviae Radix. Int J Biol Macromol. 2024;276(Pt 1):133459.
  19. Jeon J, Park KA, Lee H, et al. Water Extract of Cynanchi Atrati Radix Regulates Inflammation and Apoptotic Cell Death Through Suppression of IKK-mediated NF-κB Signaling. J Ethnopharmacol. 2011;137(1):626-34.
  20. Choi YY, Kim MH, Lee H, et al. Cynanchum Atratum Inhibits the Development of Atopic Dermatitis in 2,4-Dinitrochlorobenzene-Induced Mice. Biomed Pharmacother. 2017;90:321-327.
  21. Nitthikan N, Preedalikit W, Supadej K, et al. Exploring the Wound Healing Potential of a Cuscuta Chinensis Extract-Loaded Nanoemulsion-Based Gel. Pharmaceutics. 2024;16(5):573.
  22. Liao JC, Chang WT, Lee MS, et al. Antinociceptive and Anti-Inflammatory Activities of Cuscuta Chinensis Seeds in Mice. Am J Chin Med. 2014;42(1):223-42.
  23. Gao JM, Li R, Zhang L, et al. Cuscuta Chinensis Seeds Water Extraction Protecting Murine Osteoblastic MC3T3-E1 Cells Against Tertiary Butyl Hydroperoxide Induced Injury. J Ethnopharmacol. 2013;148(2):587-95.
  24. Han XY, Xu N, Yuan JF, et al. Total Flavonoids of Astragalus Inhibit Activated CD4+ T Cells and Regulate Differentiation of Th17/Th1/Treg Cells in Experimental Autoimmune Encephalomyelitis Mice by JAK/STAT and NF-κB Signaling Pathways. Am J Chin Med. 2023;51(5):1233-1248.
  25. Qi Y, Gao F, Hou L, Wan C. Anti-Inflammatory and Immunostimulatory Activities of Astragalosides. Am J Chin Med. 2017;45(6):1157-1167.
  26. Kang H, Ahn KS, Cho C, Bae HS. Immunomodulatory Effect of Astragali Radix Extract on Murine TH1/TH2 Cell Lineage Development. Biol Pharm Bull. 2004;27(12):1946-50.
  27. Yu WY, Li L, Wu F, et al. Moslea Herba Flavonoids Alleviated Influenza A Virus-Induced Pulmonary Endothelial Barrier Disruption via Suppressing NOX4/NF-κB/MLCK Pathway. J Ethnopharmacol. 2020;253:112641.
  28. Feng Y, Ge Q, Gao J, et al. Antiviral Activity and Underlying Mechanism of Moslae Herba Aqueous Extract for Treating SARS-CoV-2. Molecules. 2025;30(2):387.
  29. Guo J, Liu H, Jin T, et al. Moslae Herba Extract Alleviates Hyperuricemia by Regulating Uric Acid Metabolism and Relieving Renal Inflammation and Fibrosis in Mice. Phytomedicine. 2025;145:156974.
  30. Li L, Wang Z, Zhang W, et al. Isolation, Structures, and Bioactivities of Polysaccharides From Achyranthes Bidentata: A Review. Molecules. 2025;30(12):2523.
  31. Cao S, Zhang Z, Du X, et al. Extraction, Structure and Bioactivities of Polysaccharide From Achyranthes Bidentata: A Review. Carbohydr Res. 2026.
  32. Lei YY, Ye YH, Liu Y, et al. Achyranthes Bidentata Polysaccharides Improve Cyclophosphamide-Induced Adverse Reactions by Regulating the Balance of Cytokines in Helper T Cells. Int J Biol Macromol. 2024;265(Pt 2):130736.
  33. Zou Y, Meng J, Chen W, et al. Modulation of Phenotypic and Functional Maturation of Murine Dendritic Cells (DCs) by Purified Achyranthes Bidentata Polysaccharide (ABP). Int Immunopharmacol. 2011;11(8):1103-8.
  34. Ou N, Sun Y, Zhou S, et al. Evaluation of Optimum Conditions for Achyranthes Bidentata Polysaccharides Encapsulated in Cubosomes and Immunological Activity in Vitro. Int J Biol Macromol. 2018.
  35. Guo D, Mu W, Shen F, et al. Achyranthes Bidentata Polysaccharides Alleviates Rheumatoid Arthritis via the Gut Microbiota-Barrier-Metabolite Axis in Vitro and in Vivo. Int J Biol Macromol. 2025.
  36. Zhu X, Pan Y, Zheng L, Cui L, Cao Y. Polysaccharides From the Chinese Medicinal Herb Achyranthes Bidentata Enhance Anti-Malarial Immunity During Plasmodium Yoelii 17XL Infection in Mice. Malar J. 2012;11:49.
  37. Jia W, He X, Jin W, et al. Ramulus Cinnamomi Essential Oil Exerts an Anti-Inflammatory Effect on RAW264.7 Cells Through N-Acylethanolamine Acid Amidase Inhibition. J Ethnopharmacol. 2023. PMID 37311500.
  38. Liu J, Zhang Q, Chen Y, et al. Integrated Experimental Approach, Phytochemistry, and Network Pharmacology to Explore the Potential Mechanisms of Cinnamomi Ramulus for Rheumatoid Arthritis. Oxid Med Cell Longev. 2022;2022:6060677.
  39. Yu T, Lee S, Yang WS, et al. The Ability of an Ethanol Extract of Cinnamomum Cassia to Inhibit Src and Spleen Tyrosine Kinase Activity Contributes to Its Anti-Inflammatory Action. J Ethnopharmacol. 2012;139(2):566-573.
  40. Ma J, Chen X, Xue R, et al. Cinnamaldehyde Inhibits Cytokine Storms Induced by the ORF3a Protein of SARS-CoV-2 via ROS-Elimination in Activated T Cells. Phytother Res. 2023.
  41. Kim DG, Chong JE, Song Y, et al. Distinct Anti-Inflammatory Activities of Bioavailable Forms of Cinnamaldehyde and Cinnamon Polyphenols: Insight From Serum-Based, Ex Vivo, and in Vivo Analyses. J Ethnopharmacol. 2025. PMID 41421402.
  42. Song Y, Jung YS, Park S, et al. Anti-Inflammatory Effects and Macrophage Activation Induced by Bioavailable Cinnamon Polyphenols in Mice. Mol Nutr Food Res. 2023.
  43. Yang T, Jia M, Meng J, Wu H, Mei Q. Immunomodulatory Activity of Polysaccharide Isolated From Angelica Sinensis. Int J Biol Macromol. 2006;39(4-5):179-84.
  44. Wang J, Ge B, Li Z, Guan F, Li F. Structural Analysis and Immunoregulation Activity Comparison of Five Polysaccharides From Angelica Sinensis. Carbohydr Polym. 2016;140:6-12.
  45. Chen Y, Duan JA, Qian D, et al. Assessment and Comparison of Immunoregulatory Activity of Four Hydrosoluble Fractions of Angelica Sinensis in Vitro on the Peritoneal Macrophages in ICR Mice. Int Immunopharmacol. 2010;10(4):422-30.
  46. Liu Y, Song H, Li J, et al. Structural Characterization and in Vitro Antioxidant and Immunomodulatory Activities of a Water-Soluble Polysaccharide From Angelica Sinensis (ASP-4). Int J Biol Macromol. 2026.
  47. Gu P, Cai G, Yang Y, et al. Polyethylenimine-Coated PLGA Nanoparticles Containing Angelica Sinensis Polysaccharide Promote Dendritic Cells Activation and Associated Molecular Mechanisms. Int J Biol Macromol. 2022.
  48. Shen J, Zhang M, Zhang K, et al. Effect of Angelica Polysaccharide on Mouse Myeloid-Derived Suppressor Cells. Front Immunol. 2022;13:989230.
  49. Ren C, Luo Y, Li X, et al. Pharmacological Action of Angelica Sinensis Polysaccharides: A Review. Front Pharmacol. 2024.
  50. Song J, Sun H, Li Z, et al. Angelica Sinensis as a Multi-Targeted Natural Product Candidate: Constituent-Specific Mechanisms, Exposure Constraints, and Translational Development Challenges. Pharmaceuticals. 2026.
  51. Zhang L, Wei W. Anti-Inflammatory and Immunoregulatory Effects of Paeoniflorin and Total Glucosides of Paeony. Pharmacol Ther. 2020;207:107452.
  52. Jiang H, Li J, Wang L, et al. Total Glucosides of Paeony: A Review of Its Phytochemistry, Role in Autoimmune Diseases, and Mechanisms of Action. J Ethnopharmacol. 2020;258:112913.
  53. Zhou YX, Gong XH, Zhang H, Peng C. A Review on the Pharmacokinetics of Paeoniflorin and Its Anti-Inflammatory and Immunomodulatory Effects. Biomed Pharmacother. 2020;130:110505.
  54. He DY, Dai SM. Anti-Inflammatory and Immunomodulatory Effects of Paeonia Lactiflora Pall., a Traditional Chinese Herbal Medicine. Front Pharmacol. 2011;2:10.
  55. Zhang W, Dai SM. Mechanisms Involved in the Therapeutic Effects of Paeonia Lactiflora Pallas in Rheumatoid Arthritis. Int Immunopharmacol. 2012;14(1):27-31.
  56. Liu J, Chen S, Zhang Z, et al. The Oxidized Hyaluronic Acid Hydrogels Containing Paeoniflorin Microspheres Regulates the Polarization of M1/M2 Macrophages to Promote Wound Healing. Int J Biol Macromol. 2024;282(Pt 5):137107.
  57. Feng R, Tian F, Zhou J, et al. A Preliminary Study on the Promotion of Wound Healing by Paeoniflorin Carbon Dots Loaded in Chitosan Hydrogel. Biomed Mater. 2025;20(3).
  58. Xie XD, Tang M, Yi SL, et al. Polysaccharide of Asparagus Cochinchinensis (Lour.) Merr Regulates Macrophage Immune Response and Epigenetic Memory Through TLR4-JNK/p38/ERK Signaling Pathway and Histone Modification. Phytomedicine. 2023;124:155294.
  59. Wang L, Zhang Z, Zhao W, et al. Physicochemical, Rheological, Antioxidant and Immunological Properties of Four Novel Non-Inulin (Poly)saccharides From Asparagus Cochinchinensis. Int J Biol Macromol. 2023;258(Pt 2):129034.
  60. Lee HA, Koh EK, Sung JE, et al. Ethyl Acetate Extract From Asparagus cochinchinensis Exerts Anti-inflammatory Effects in LPS-stimulated RAW264.7 Macrophage Cells by Regulating COX-2/iNOS, Inflammatory Cytokine Expression, MAP Kinase Pathways, the Cell Cycle and Anti-Oxidant Activity. Mol Med Rep. 2017;15(4):1613-1623.
  61. Lee JH, Lim HJ, Lee CW, et al. Methyl Protodioscin From the Roots of Asparagus Cochinchinensis Attenuates Airway Inflammation by Inhibiting Cytokine Production. Evid Based Complement Altern Med. 2015;2015:640846.
  62. Fan Y, Ma X, Ma L, et al. Antioxidative and Immunological Activities of Ophiopogon Polysaccharide Liposome From the Root of Ophiopogon Japonicus. Carbohydr Polym. 2016;135:110-20.
  63. Li J, Zhou L, Xiao Z. Advances in the Study of Ophiopogon Japonicus Polysaccharides: Structural Characterization, Bioactivity and Gut Microbiota Modulation Regulation. Front Pharmacol. 2025;16:1583711.
  64. Sun W, Hu W, Meng K, et al. Activation of Macrophages by the Ophiopogon Polysaccharide Liposome From the Root Tuber of Ophiopogon Japonicus. Int J Biol Macromol. 2016;91:918-25.
  65. Cui J, Pan X, Duan X, et al. Ophiopogon Polysaccharide Liposome Regulated the Immune Activity of Kupffer Cell Through miR-4796. Int J Mol Sci. 2022;23(23):14659.
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