Anti-Inflammatory and Anti-Allergic Effects of Saponarin and Its Impact on Signaling Pathways of RAW 264.7, RBL-2H3, and HaCaT Cells.
Min. Seon-Young SY; Park. Che-Hwon CH; Yu. Hye-Won HW; Park. Young-Jin YJ
Key Findings
- In mouse macrophage cells, 80 µM saponarin sharply lowered inflammatory cytokines (TNF‑α, IL‑1β) and blocked ERK/p38 signaling.
- In rat basophil‑like cells, 40 µM saponarin reduced allergic degranulation and cut a range of cytokines by inhibiting Syk, PLCγ1, ERK, JNK and p38 pathways.
- In human keratinocyte cells, 100 µM saponarin decreased chemokines and STAT1 activation while increasing skin‑barrier factors hyaluronan synthase‑3, aquaporin‑3 and the antimicrobial peptide LL‑37.
Practical Outcomes
- Saponarin could be explored as a topical or oral ingredient for calming skin inflammation or atopic dermatitis, but human dosing and safety are not established yet. Biohackers might try barley‑leaf extracts that contain saponarin, starting with low doses and watching for skin improvements, while awaiting clinical data.
Summary
Saponarin, a flavone from young barley leaves, was shown in lab cell studies to calm down inflammation and allergic reactions and to boost skin‑protective proteins like LL‑37, hyaluronan synthase‑3 and aquaporin‑3. While the work is all in petri dishes, it hints that saponarin‑rich extracts might help skin health and reduce irritation.
Abstract
Saponarin{5-hydroxy-2-(4-hydroxyphenyl)-6-[3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]-7-[3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-4-one}, a flavone found in young green barley leaves, is known to possess antioxidant, antidiabetic, and hepatoprotective effects. In the present study, the anti-inflammatory, anti-allergic, and skin-protective effects of saponarin were investigated to evaluate its usefulness as a functional ingredient in cosmetics. In lipopolysaccharide-induced RAW264.7 (murine macrophage) cells, saponarin (80 μM) significantly inhibited cytokine expression, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, inducible nitric oxide synthase, and cyclooxygenase (COX)-2. Saponarin (80 μM) also inhibited the phosphorylation of extracellular signal-regulated kinase (ERK) and p38 involved in the mitogen-activated protein kinase signaling pathway in RAW264.7 cells. Saponarin (40 μM) significantly inhibited β-hexosaminidase degranulation as well as the phosphorylation of signaling effectors (Syk, phospholipase Cγ1, ERK, JNK, and p38) and the expression of inflammatory mediators (tumor necrosis factor [TNF]-α, IL-4, IL-5, IL-6, IL-13, COX-2, and FcεRIα/γ) in DNP-IgE- and DNP-BSA-stimulated RBL-2H3 (rat basophilic leukemia) cells. In addition, saponarin (100 μM) significantly inhibited the expression of macrophage-derived chemokine, thymus and activation-regulated chemokine, IL-33, thymic stromal lymphopoietin, and the phosphorylation of signaling molecules (ERK, p38 and signal transducer and activator of transcription 1 [STAT1]) in TNF-α- and interferon (IFN)-γ-stimulated HaCaT (human immortalized keratinocyte) cells. Saponarin (100 μM) also significantly induced the expression of hyaluronan synthase-3, aquaporin 3, and cathelicidin antimicrobial peptide (LL-37) in HaCaT cells, which play an important role as skin barriers. Saponarin remarkably inhibited the essential factors involved in the inflammatory and allergic responses of RAW264.7, RBL-2H3, and HaCaT cells, and induced the expression of factors that function as physical and chemical skin barriers in HaCaT cells. Therefore, saponarin could potentially be used to prevent and relieve immune-related skin diseases, including atopic dermatitis.
Study Information
pubmed
2021
2021-08-05T00:00:00.000Z
10.3390/ijms22168431
41
102