scholarly journals Glycyrrhizic acid from licorice down-regulates inflammatory responses via blocking MAPK and PI3K/Akt-dependent NF-κB signalling pathways in TPA-induced skin inflammation

MedChemComm ◽  
2018 ◽  
Vol 9 (9) ◽  
pp. 1502-1510 ◽  
Author(s):  
Wenfeng Liu ◽  
Shun Huang ◽  
Yonglian Li ◽  
Yanwen Li ◽  
Dongli Li ◽  
...  
Keyword(s):  
Glycyrrhizic Acid ◽  
Inflammatory Responses ◽  
Principal Component ◽  
Skin Inflammation ◽  
Signalling Pathways ◽  
Glycyrrhizinic Acid

Glycyrrhizinic acid (GA), a principal component derived from licorice, is attracting considerable attention because of its broad range of bioactivities.

scholarly journals Diversified Stimuli-Induced Inflammatory Pathways Cause Skin Pigmentation

2021 ◽  
Vol 22 (8) ◽  
pp. 3970
Author(s):  
Md Razib Hossain ◽  
Tuba M. Ansary ◽  
Mayumi Komine ◽  
Mamitaro Ohtsuki
Keyword(s):  
Inflammatory Responses ◽  
Light Exposure ◽  
Skin Pigmentation ◽  
Basal Layer ◽  
Decisive Role ◽  
Skin Inflammation ◽  
Dermal Fibroblasts ◽  
Epidermal Keratinocytes ◽  
Hair Color ◽  
Microbial Infection

The production of melanin pigments by melanocytes and their quantity, quality, and distribution play a decisive role in determining human skin, eye, and hair color, and protect the skin from adverse effects of ultraviolet radiation (UVR) and oxidative stress from various environmental pollutants. Melanocytes reside in the basal layer of the interfollicular epidermis and are compensated by melanocyte stem cells in the follicular bulge area. Various stimuli such as eczema, microbial infection, ultraviolet light exposure, mechanical injury, and aging provoke skin inflammation. These acute or chronic inflammatory responses cause inflammatory cytokine production from epidermal keratinocytes as well as dermal fibroblasts and other cells, which in turn stimulate melanocytes, often resulting in skin pigmentation. It is confirmed by some recent studies that several interleukins (ILs) and other inflammatory mediators modulate the proliferation and differentiation of human epidermal melanocytes and also promote or inhibit expression of melanogenesis-related gene expression directly or indirectly, thereby participating in regulation of skin pigmentation. Understanding of mechanisms of skin pigmentation due to inflammation helps to elucidate the relationship between inflammation and skin pigmentation regulation and can guide development of new therapeutic pathways for treating pigmented dermatosis. This review covers the mechanistic aspects of skin pigmentation caused by inflammation.

scholarly journals A Novel Combination of Vitamin C, Curcumin and Glycyrrhizic Acid Potentially Regulates Immune and Inflammatory Response Associated with Coronavirus Infections: A Perspective from System Biology Analysis

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1193 ◽  
Author(s):  
Liang Chen ◽  
Chun Hu ◽  
Molly Hood ◽  
Xue Zhang ◽  
Lu Zhang ◽  
...  
Keyword(s):  
Immune Response ◽  
Vitamin C ◽  
Inflammatory Response ◽  
Signaling Pathways ◽  
System Biology ◽  
Glycyrrhizic Acid ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Gene Target

Novel coronaviruses (CoV) have emerged periodically around the world in recent years. The recurrent spreading of CoVs imposes an ongoing threat to global health and the economy. Since no specific therapy for these CoVs is available, any beneficial approach (including nutritional and dietary approach) is worth investigation. Based on recent advances in nutrients and phytonutrients research, a novel combination of vitamin C, curcumin and glycyrrhizic acid (VCG Plus) was developed that has potential against CoV infection. System biology tools were applied to explore the potential of VCG Plus in modulating targets and pathways relevant to immune and inflammation responses. Gene target acquisition, gene ontology and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment were conducted consecutively along with network analysis. The results show that VCG Plus can act on 88 hub targets which are closely connected and associated with immune and inflammatory responses. Specifically, VCG Plus has the potential to regulate innate immune response by acting on NOD-like and Toll-like signaling pathways to promote interferons production, activate and balance T-cells, and regulate the inflammatory response by inhibiting PI3K/AKT, NF-κB and MAPK signaling pathways. All these biological processes and pathways have been well documented in CoV infections studies. Therefore, our findings suggest that VCG Plus may be helpful in regulating immune response to combat CoV infections and inhibit excessive inflammatory responses to prevent the onset of cytokine storm. However, further in vitro and in vivo experiments are warranted to validate the current findings with system biology tools. Our current approach provides a new strategy in predicting formulation rationale when developing new dietary supplements.

scholarly journals Dietary Vitamin D Increases Percentages and Function of Regulatory T Cells in the Skin-Draining Lymph Nodes and Suppresses Dermal Inflammation

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Shelley Gorman ◽  
Sian Geldenhuys ◽  
Melinda Judge ◽  
Clare E. Weeden ◽  
Jason Waithman ◽  
...  
Keyword(s):  
Vitamin D ◽  
Lymph Nodes ◽  
Chemokine Receptors ◽  
Inflammatory Responses ◽  
Skin Inflammation ◽  
Dietary Vitamin ◽  
Suppressive Activity ◽  
Mesenteric Lymph Nodes ◽  
Dietary Vitamin D ◽  
Draining Lymph Nodes

Skin inflammatory responses in individuals with allergic dermatitis may be suppressed by dietary vitamin D through induction and upregulation of the suppressive activity of regulatory T (TReg) cells. Vitamin D may also promoteTRegcell tropism to dermal sites. In the current study, we examined the capacity of dietary vitamin D3to modulate skin inflammation and the numbers and activity ofTRegcells in skin and other sites including lungs, spleen, and blood. In female BALB/c mice, dietary vitamin D3suppressed the effector phase of a biphasic ear swelling response induced by dinitrofluorobenzene in comparison vitamin D3-deficient female BALB/c mice. Vitamin D3increased the percentage ofTReg(CD3+CD4+CD25+Foxp3+) cells in the skin-draining lymph nodes (SDLN). The suppressive activity ofTRegcells in the SDLN, mesenteric lymph nodes, spleen, and blood was upregulated by vitamin D3. However, there was no difference in the expression of the naturally occurringTRegcell marker, neuropilin, nor the expression of CCR4 or CCR10 (skin-tropic chemokine receptors) onTRegcells in skin, SDLN, lungs, and airway-draining lymph nodes. These data suggest that dietary vitamin D3increased the percentages and suppressive activity ofTRegcells in the SDLN, which are poised to suppress dermal inflammation.

scholarly journals TWEAK/Fn14 Activation Participates in Skin Inflammation

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Qilu Liu ◽  
Shengxiang Xiao ◽  
Yumin Xia
Keyword(s):  
Cell Fate ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Biological Activities ◽  
Inflammatory Cells ◽  
Skin Inflammation ◽  
Tnf Receptor ◽  
Inflammatory Infiltration ◽  
Papillomavirus Infection ◽  
Chemotactic Protein

Tumor necrosis factor- (TNF-) like weak inducer of apoptosis (TWEAK) participates in multiple biological activities via binding to its sole receptor—fibroblast growth factor-inducible 14 (Fn14). The TWEAK/Fn14 signaling pathway is activated in skin inflammation and modulates the inflammatory responses of keratinocytes by activating nuclear factor-κB signals and enhancing the production of several cytokines, including interleukins, monocyte chemotactic protein-1, RANTES (regulated on activation, normal T cell expressed and secreted), and interferon gamma-induced protein 10. Mild or transient TWEAK/Fn14 activation contributes to tissular repair and regeneration while excessive or persistent TWEAK/Fn14 signals may lead to severe inflammatory infiltration and tissue damage. TWEAK also regulates cell fate of keratinocytes, involving the function of Fn14-TNF receptor-associated factor-TNF receptor axis. By recruiting inflammatory cells, promoting cytokine production, and regulating cell fate, TWEAK/Fn14 activation plays a pivotal role in the pathogenesis of various skin disorders, such as psoriasis, atopic dermatitis, cutaneous vasculitis, human papillomavirus infection and related skin tumors, and cutaneous autoimmune diseases. Therefore, the TWEAK/Fn14 pathway may be a potential target for the development of novel therapeutics for skin inflammatory diseases.

scholarly journals Glycyrrhizic acid suppresses Cox-2-mediated anti-inflammatory responses during Leishmania donovani infection

2012 ◽  
Vol 67 (8) ◽  
pp. 1905-1914 ◽  
Author(s):  
S. Bhattacharjee ◽  
A. Bhattacharjee ◽  
S. Majumder ◽  
S. B. Majumdar ◽  
S. Majumdar
Keyword(s):  
Leishmania Donovani ◽  
Glycyrrhizic Acid ◽  
Inflammatory Responses ◽  
Cox 2 ◽  
Anti Inflammatory

scholarly journals An Important Role of Blood and Lymphatic Vessels in Inflammation and Allergy

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Silvana Zgraggen ◽  
Alexandra M. Ochsenbein ◽  
Michael Detmar
Keyword(s):  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Experimental Studies ◽  
Lymphatic Vessels ◽  
Allergic Inflammation ◽  
Skin Inflammation ◽  
Chronic Inflammatory Diseases ◽  
Chronic Skin ◽  
Targeted Inhibition ◽  
Endothelial Growth Factor

Angiogenesis and lymphangiogenesis, the growth of new vessels from preexisting ones, have received increasing interest due to their role in tumor growth and metastatic spread. However, vascular remodeling, associated with vascular hyperpermeability, is also a key feature of many chronic inflammatory diseases including asthma, atopic dermatitis, psoriasis, and rheumatoid arthritis. The major drivers of angiogenesis and lymphangiogenesis are vascular endothelial growth factor- (VEGF-)A and VEGF-C, activating specific VEGF receptors on the lymphatic and blood vascular endothelium. Recent experimental studies found potent anti-inflammatory responses after targeted inhibition of activated blood vessels in models of chronic inflammatory diseases. Importantly, our recent results indicate that specific activation of lymphatic vessels reduces both acute and chronic skin inflammation. Thus, antiangiogenic and prolymphangiogenic therapies might represent a new approach to treat chronic inflammatory disorders, including those due to chronic allergic inflammation.

Preparation and Evaluation of Calcium Alginate/Glycyrrhizic Acid Hydrogel

2014 ◽  
Vol 941-944 ◽  
pp. 1065-1068
Author(s):  
Ying Zong Ren ◽  
Yi Zhang ◽  
Li Na Gao ◽  
Yuan Lu Cui ◽  
Yun Qi
Keyword(s):  
Calcium Alginate ◽  
Glycyrrhizic Acid ◽  
Inflammatory Responses ◽  
Gelation Time ◽  
Alginate Hydrogel ◽  
Hybrid Hydrogel ◽  
Alginate Solution ◽  
Gelling Time ◽  
Calcium Alginate Hydrogel ◽  
Preparation And Evaluation

Calcium ions released from calcium-alginate hydrogel can promote inflammatory responses when injected subcutaneously in mice. In this study, a novel alginate hybrid hydrogel was prepared using sodium alginate (SA) and Glycyrrhizic acid (GA) design for reduce calcium concentration in the hydrogel. nanoCalcium carbonate was wrapped in an alginate solution and internal gelling was induced by the Ca2+ released from CaCO3 by adding of GA. As varying of the amounts of GA and CaCO3 in alginate solution, the gelling time could be controlled within 10 min. Taking advantage of short gelation time and controlled hydrogel shape, GA calcium alginate hydrogel system has great potential for tissue engineering applications.

scholarly journals NF-κB/AP-1-Targeted Inhibition of Macrophage-Mediated Inflammatory Responses by Depigmenting Compound AP736 Derived from Natural 1,3-Diphenylpropane Skeleton

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Van Thai Ha ◽  
Heung Soo Beak ◽  
Eunji Kim ◽  
Kwang-Soo Baek ◽  
Muhammad Jahangir Hossen ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Morphological Changes ◽  
Skin Inflammation ◽  
No Synthase ◽  
Raw264.7 Cells ◽  
Inflammatory Gene Expression ◽  
Anti Inflammatory ◽  
Targeted Inhibition ◽  
Tyrosinase Expression ◽  
Phagocytic Uptake

AP736 was identified as an antimelanogenic drug that can be used for the prevention of melasma, freckles, and dark spots in skin by acting as a suppressor of melanin synthesis and tyrosinase expression. Since macrophage-mediated inflammatory responses are critical for skin health, here we investigated the potential anti-inflammatory activity of AP736. The effects of AP736 on various inflammatory events such as nitric oxide (NO)/prostaglandin (PG) E2production, inflammatory gene expression, phagocytic uptake, and morphological changes were examined in RAW264.7 cells. AP736 was found to strongly inhibit the production of both NO and PGE2in lipopolysaccharide- (LPS-) treated RAW264.7 cells. In addition, AP736 strongly inhibited both LPS-induced morphological changes and FITC-dextran-induced phagocytic uptake. Furthermore, AP736 also downregulated the expression of multiple inflammatory genes, such as inducible NO synthase (iNOS), cyclooxygenase- (COX-) 2, and interleukin- (IL-) 1βin LPS-treated RAW264.7 cells. Transcription factor analysis, including upstream signalling events, revealed that both NF-κB and AP-1 were targeted by AP736 via inhibition of the IKK/IκBαand IRAK1/TAK1 pathways. Therefore, our results strongly suggest that AP736 is a potential anti-inflammatory drug due to its suppression of NF-κB-IKK/IκBαand AP-1-IRAK1/TAK1 signalling, which may make AP736 useful for the treatment of macrophage-mediated skin inflammation.

scholarly journals Identification of Axl as a downstream effector of TGF-β1 during Langerhans cell differentiation and epidermal homeostasis

2012 ◽  
Vol 209 (11) ◽  
pp. 2033-2047 ◽  
Author(s):  
Thomas Bauer ◽  
Anna Zagórska ◽  
Jennifer Jurkin ◽  
Nighat Yasmin ◽  
René Köffel ◽  
...  
Keyword(s):  
Transforming Growth Factor ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Apoptotic Cell ◽  
Skin Inflammation ◽  
Transforming Growth Factor Β1 ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
And Function ◽  
Tgf Β1

Transforming growth factor-β1 (TGF-β1) is a fundamental regulator of immune cell development and function. In this study, we investigated the effects of TGF-β1 on the differentiation of human Langerhans cells (LCs) and identified Axl as a key TGF-β1 effector. Axl belongs to the TAM (Tyro3, Axl, and Mer) receptor tyrosine kinase family, whose members function as inhibitors of innate inflammatory responses in dendritic cells and are essential to the prevention of lupus-like autoimmunity. We found that Axl expression is induced by TGF-β1 during LC differentiation and that LC precursors acquire Axl early during differentiation. We also describe prominent steady-state expression as well as inflammation-induced activation of Axl in human epidermal keratinocytes and LCs. TGF-β1–induced Axl enhances apoptotic cell (AC) uptake and blocks proinflammatory cytokine production. The antiinflammatory role of Axl in the skin is reflected in a marked impairment of the LC network preceding spontaneous skin inflammation in mutant mice that lack all three TAM receptors. Our findings highlight the importance of constitutive Axl expression to tolerogenic barrier immunity in the epidermis and define a mechanism by which TGF-β1 enables silent homeostatic clearing of ACs to maintain long-term self-tolerance.

scholarly journals Microbiota instruct IL-17A-producing innate lymphoid cells to promote skin inflammation in cutaneous leishmaniasis

2021 ◽  
Author(s):  
Tej Pratap Singh ◽  
Augusto Carvalho ◽  
Elizabeth Grice ◽  
Phillip Scott
Keyword(s):  
Cutaneous Leishmaniasis ◽  
Staphylococcus Epidermidis ◽  
Leishmania Major ◽  
Inflammatory Responses ◽  
Skin Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Skin Microbiota ◽  
Infected Skin

p.p1 {margin: 0.0px 0.0px 0.0px 0.0px; font: 12.0px Helvetica} span.s1 {color: #222222} span.s2 {font: 8.0px Helvetica} Innate lymphoid cells (ILCs) comprise a heterogeneous population of immune cells that maintain barrier function and can initiate a protective or pathological immune response upon infection. Here we show the involvement of IL-17A-producing ILCs in microbiota-driven immunopathology in cutaneous leishmaniasis. IL-17A-producing ILCs were RORgt + and were enriched in Leishmania major infected skin, and topical colonization with Staphylococcus epidermidis before L. major infection exacerbated the skin inflammatory responses and IL-17A-producing RORgt + ILC accumulation without impacting type 1 immune responses. IL-17A responses in ILCs were directed by Batf3 dependent CD103 + dendritic cells, and experiments using ILC deficient Rag1 -/- mice established that IL-17A + ILCs were sufficient in driving the inflammatory responses. As depletion of ILCs or neutralization of IL-17A diminished the microbiota mediated immunopathology. Taken together, this study indicates that the skin microbiota promotes RORgt + IL-17A-producing ILCs, which augment the skin inflammation in cutaneous leishmaniasis.

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