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Function

Tangs Vitigo is a botanical compound formulated to assist the body expelling of feng, activating blood circulation and invigorating qi & meridians, it also helps to nourish the gan & shen to facilitate detoxification process, thus enhancing the immune system. Its ingredients contains of 100% natural botanicals.

Indications

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

  • Erythrodermic Psoriasis patients must consult doctor before starting treatment

Contraindications

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

During Tangs Vitigo therapy, all immunosuppressants therapy is stopped. Patients with a history of immunosuppressant use will likely start to experience the so-called Wavelike Flare-up Cycle (Fig.1). This is known as the Immunosuppressant Withdrawal Syndrome. Symptoms of skin diseases which had previously been suppressed by immunotherapy will start to resurface with vigor after the immune system is no longer being curtailed. Over time, as Tangs Vitigo gradually takes effect in correcting the immune system’s function, the flare-ups will subside in frequency and intensity in a wavelike pattern (Fig 1). The time to reach the endpoint where the wave draws to a null, will depend on the dosage and potency of the immunosuppressants that the user had formerly consumed.

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.
  • 皮质类固醇等免疫抑制剂药物 (包括UVB和PUVA) 和植物类免疫抑制剂药物 (甘草,白鲜皮,蝉蜕,大黄,金银花,雷公藤等),口服避孕药,饮酒,熬夜,刺激癣疹(搔抓搓),精神情绪不稳定,热水洗浴.

Ingredients

Tangs Vitigo-1, each 360mg extract equivalent raw herbs:
Radix et rhizoma salviae miltiorrhizae [1-4] 250mg
Lignum dalbergiae odoriferae [5,6] 500mg
Flos carthami  [7] 625mg
Radix Saposhnikoviae Divaricatae [8-12]  333mg
Radix et rhizoma cynanchii atrati [13,14] 125mg
Semen cuscutae [15-18] 333mg
Radix astragali [19-23]  255mg
Herba moslae [24-35]  125mg
Radix achyranthis bidentatae [36-39] 333mg
Ramulus cinnamomi [40,41] 333mg

Tangs Vitigo-2, each 360mg extract equivalent raw herbs:
Radix Angelica sinensis [42-45] 200mg
Radix Paeonia lactiflora [46-53] 200mg
Radix Asparogus cochinchinensis [54-57] 333mg
Radix Ophiopogon japonicus [58-62] 333mg
Radix et rhizoma salviae miltiorrhizae [1-4] 250mg
Lignum dalbergiae odoriferae [5,6] 333mg
Flos carthami [7] 600mg
Radix Saposhnikoviae Divaricatae [8-12]  333mg
Radix et rhizoma cynanchii atrati [13,14] 200mg
Semen cuscutae [15-18] 333mg

Clinical Evidence

Radix Salviae Miltiorrhizae [1-4] bioactive compounds tanshinones I and IIA suppress Th1 differentiation and function, primarily by inhibiting STAT3/STAT5 phosphorylation, leading to reduced IFN-γ production and Th1-mediated inflammation. Salvianolic acid A and tanshinone IIA decrease Th2 cytokines (IL-4, IL-13) in allergic asthma models, indicating inhibition of Th2 responses and potential anti-allergic effects. Tanshinones inhibit Th17 differentiation and function, likely via STAT pathway blockade, which may reduce IL-17-mediated inflammation in autoimmune diseases. Polysaccharides from Salvia miltiorrhiza promote Treg differentiation and function, enhancing immune tolerance and potentially mitigating autoimmunity, and enhance CD8+ T cell cytotoxicity and promote tumor cell apoptosis, supporting anti-tumor immunity.

Dalbergia odorifera [5,6] have been shown to accelerate wound closure, enhance tissue quality, and reduce inflammation and oxidative stress in animal models. The active compounds identified—such as butin, eriodyctiol, and formononetin—facilitate wound healing by modulating the PI3K/Akt signaling pathway and upregulating growth factors including TGF-β1, FGF2, VEGFA, ECM1, and α-SMA at various stages of skin repair. These effects result in improved re-epithelialization, granulation tissue formation, and collagen deposition, while also suppressing pro-inflammatory cytokines and oxidative stress markers. Additionally, Dalbergia odorifera extracts have been found to promote keratinocyte migration and proliferation, likely through increased matrix metalloproteinase-9 (MMP-9) production and modulation of genes involved in skin homeostasis, further supporting their role in wound healing. The extracts also exhibit anti-inflammatory properties by downregulating cyclooxygenase-2, inducible nitric oxide synthase, TNF-α, and IL-6 expression.

Flos Carthami [7] increase proliferation, migration, and tube formation of human microvascular endothelial cells, which are key processes in wound healing. In vivo, Flos Carthami extract enhances angiogenesis in zebrafish, upregulating multiple genes involved in endothelial cell migration, matrix remodeling, and vessel maturation, such as VEGFR3, HIF1A, MMP2, and ANGPT1.

Radix Saposhnikoviae Divaricatae [8-12] exhibits immunomodulatory effects primarily through its polysaccharide components, which influence both innate and adaptive immune responses. The most robust evidence demonstrates that it extract can suppress Th1 differentiation and function, as shown by reduced IFN-γ production and T-bet expression, and a decreased Th1/Th2 cytokine ratio in murine models of allergic contact dermatitis. This effect is mediated in part by downregulation of dendritic cell maturation and costimulatory molecule expression, thereby limiting Th1 polarization and inflammatory infiltration.

Radix et Rhizoma Cynanchii [13,14] can suppress inflammatory mediators such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) by inhibiting IKK-mediated NF-κB signaling, which is a key pathway in the regulation of inflammation and cellular apoptosis during tissue repair. This anti-inflammatory effect is further supported by evidence of reduced pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) and decreased mast cell infiltration in models of skin inflammation, suggesting a potential role in modulating the inflammatory phase of wound healing. Additionally, Cynanchum atratum contains C21 steroidal glycosides and other bioactive compounds with antioxidant activities, which may help regulate immune responses and oxidative stress in the wound microenvironment.These mechanisms are considered beneficial for promoting tissue repair and reducing excessive inflammation that can impair healing.

Semen cuscutae [15-18] are rich in polyphenolics and flavonoids, which confer strong antioxidant potential, but the specific immunological effects depend on both the Cuscuta species and the host plant from which it is harvested. The extract exhibited antioxidant, anti-inflammatory, and antibacterial activities, including reduction of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and presence of bioactive compounds such as kaempferol and hyperoside, which are implicated in these effects, Additional mechanistic studies show that Cuscuta chinensis seed extracts can decrease inflammatory mediators and oxidative stress markers in vivo, further supporting its role in modulating inflammation and oxidative damage, both critical to wound repair.

Radix Astragali [19-23] modulates the balance between Th1, Th2, Th17, and regulatory T cells (Treg). Specifically, its flavonoids suppress Th1 and Th17 differentiation and cytokine production (e.g., IFN-γ, IL-17), while promoting Treg differentiation and function, primarily via JAK/STAT and NF-κB signaling pathways. This mechanism is relevant in autoimmune and inflammatory disease models, where shifting the Th17/Treg axis reduces pathogenic inflammation. It also influences Th2 responses, with evidence showing increased IL-4 production and reduced IFN-γ, indicating a shift toward Th2 polarization in murine models. This may be beneficial in allergic conditions, but the overall effect is context-dependent. For CD8+ T cells, Radix Astragali extracts increase the expression of CD8 and related transcription factors, supporting cytotoxic T cell activation and proliferation.

In vivo and in vitro models show that Herba moslae Moslae [24-35] flavonoids, especially luteolin and kaempferol, can attenuate acute lung injury and viral-induced pulmonary endothelial barrier dysfunction by suppressing inflammatory pathways such as NOX4/NF-κB/MLCK and MAPK, and reducing cytokine production (IL-6, TNF-α, IL-1β). These effects suggest potential utility in respiratory infections, including influenza and SARS-CoV-2, where Moslae Herba aqueous extract inhibited viral replication and modulated host gene expression relevant to COVID-19 pathogenesis.Luteolin and kaempferol, as isolated compounds, have broad pharmacological profiles. Luteolin is recognized for its anti-inflammatory, antioxidant, anticancer, neuroprotective, and cardioprotective effects, with clinical trials ongoing for chronic inflammatory and neoplastic diseases. Kaempferol similarly exhibits anti-inflammatory, antioxidant, antimicrobial, and anticancer properties, and is under investigation for its role in aging-related diseases, metabolic disorders, and cancer. Herba moslae also shows promise in metabolic disease models, such as hyperuricemia, by regulating uric acid metabolism, suppressing renal inflammation, and modulating gut microbiota.

Radix achyranthis bidentatae [36-39] exhibits immunomodulatory activity, primarily attributed to its polysaccharide components. Preclinical studies demonstrate that Achyranthes bidentata polysaccharides (ABPs) enhance both innate and adaptive immune responses by promoting lymphocyte proliferation, increasing macrophage phagocytic function, and upregulating cytokines such as IL-2, IL-6, IFN-γ, and TNF-α. ABPs also modulate helper T cell (Th) cytokine balance, particularly by increasing Th1-type responses and restoring immune organ indices in immunosuppressed animal models. ABPs have been shown to induce phenotypic and functional maturation of dendritic cells, increasing expression of MHC II, CD86, and CD40, and enhancing IL-12 production, which may contribute to improved antigen presentation and T cell activation. In infectious disease models, ABPs selectively enhance Th1-mediated immunity, increasing macrophage and dendritic cell populations and improving host resistance to pathogens.

Ramulus Cinnamomi [40,41] promotes Th1 cell recovery and suppresses Th17 and regulatory T cell (Treg) expansion following immune injury, such as low-dose total body irradiation. Mechanistically, it enhances T-bet expression (Th1 master transcription factor), increases IFN-γ production, and limits Foxp3 transcription (Treg marker), thereby shifting the balance toward Th1-mediated antitumor immunity and away from immunosuppressive Treg and pro-inflammatory Th17 responses. In models of autoimmune disease (experimental allergic encephalomyelitis), Ramulus Cinnamomi upregulates Treg populations, likely via reduction of nitric oxide production, which is associated with amelioration of disease severity. The protective effect is abrogated when Tregs are neutralized, indicating a direct role for Ramulus Cinnamomi in Treg maintenance in this context. These findings suggest context-dependent effects: it can both suppress and promote Treg populations depending on the underlying immune milieu.

Radix Angelica sinensis [42-45] contains bioactive polysaccharides that have demonstrated immunomodulatory effects in both in vitro and in vivo studies. The primary active constituents, Angelica sinensis polysaccharides (ASP), have been shown to enhance both innate and adaptive immune responses. Mechanistically, ASP promotes lymphocyte proliferation, increases macrophage phagocytic activity, and upregulates the secretion of cytokines such as IFN-γ, IL-2, IL-6, and TNF-α, indicating stimulation of Th1-type immune responses and activation of macrophages and natural killer cells. ASP also modulates the function and differentiation of myeloid-derived suppressor cells (MDSCs) via STAT1/STAT3 signaling, which may have implications for immune regulation in disease states. Additionally, ASP can upregulate Toll-like receptor 4 (TLR4) expression, further supporting its role in immune activation.

Radix Paeonia lactiflora [46-53] act on multiple intracellular signaling pathways, including NF-κB, MAPK, PI3K/Akt, and JAK/STAT, which are central to immune cell activation and inflammatory mediator production. In animal models of autoimmune diseases (e.g., rheumatoid arthritis, experimental autoimmune encephalomyelitis, and atopic dermatitis), these compounds reduce disease severity and inflammatory markers, and promote immune tolerance by shifting Th1/Th2/Th3 cell activity. Paeoniflorin, when delivered via hydrogels or carbon dot nanomaterials, accelerates wound closure in rat models by reducing inflammatory cell infiltration, promoting re-epithelialization, increasing collagen deposition, and shifting macrophage polarization from the pro-inflammatory M1 phenotype to the reparative M2 phenotype. In diabetic wound models, paeonol combined with stem cell-derived exosomes in a thermosensitive hydrogel enhances wound healing by promoting epithelial-mesenchymal transition (EMT) and angiogenesis, mediated through upregulation of miR-424-5p. This results in increased proliferation and migration of fibroblasts and endothelial cells, improved vascularization, and faster re-epithelialization.

Radix Asparogus cochinchinensis [54-57] modulates immunity by both stimulating macrophage-mediated innate immune responses and suppressing pathological inflammation. The bioactive polysaccharides, oligosaccharides, and steroidal saponins that exert immunomodulatory effects primarily by regulating macrophage function and inflammatory cytokine production. Polysaccharides from this root have been shown to activate macrophages via the TLR4-MAPK (JNK/p38/ERK) signaling pathway, leading to increased expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6, and promoting innate immune memory through histone modification (notably H3K4me1). Its specific compounds (e.g., methyl protodioscin) suppress excessive inflammatory responses by inhibiting the production of nitric oxide, COX-2, and reactive oxygen species, and downregulating cytokine expression in activated macrophages and epithelial cells.

Radix Ophiopogon japonicus [58-62] have been shown to increase splenocyte proliferation, promote the proportion of CD4+ and CD8+ T cells, elevate cytokine production, and improve antigen-specific antibody titers in animal models, indicating broad immunostimulatory effects. Ophiopogon liposomal formulations (OPL) activate macrophages, increasing phagocytic activity, nitric oxide production, and the expression of immune-related surface molecules (CD14, MHC-II), as well as upregulating pro-inflammatory cytokines such as IL-1β and TNF-α. These effects are mediated, at least in part, through the TLR4-NF-κB signaling pathway and modulation of microRNAs such as miR-4796. Ophiopogon japonicus have also been shown to counteract immunosuppression in animal models, restoring immune cell numbers and cytokine levels after cyclophosphamide-induced immunosuppression.

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