Woon Sang Hwang

Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by epidermal barrier dysfunction and dysregulated immune responses, particularly an imbalance between T helper type 1 (Th1) and type 2 (Th2) cytokines. Natural products with immunomodulatory activity have attracted increasing attention as potential strategies for regulating allergic inflammation. In this study, we investigated the immunomodulatory effects of bioprocessed black rice bran (BRB-F) and bioprocessed balloon flower root (BFR-F). In vitro assays using human B cells, mast cells, and keratinocytes were conducted to evaluate IgE production, mast cell degranulation, and epithelial inflammatory mediator release. The efficacy of the BRB-F:BFR-F mixture was further evaluated in BALB/c mice with 2,4-dinitrochlorobenzene (DNCB)/Dermatophagoides farinae extract (DFE)-induced AD-like dermatitis. BRB-F and BFR-F suppressed IgE production, attenuated mast cell degranulation and thymic stromal lymphopoietin (TSLP) release, and reduced keratinocyte-derived inflammatory mediators (thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC), and IL-6). In mice, dietary supplementation with the BRB-F:BFR-F mixture (10–80 mg/kg/day) dose-dependently improved clinical skin lesions and histopathological changes, with serum IgE reduced by up to 87.1% at the highest dose. The treatment significantly suppressed Th2 cytokine mRNA expression in ear tissue (IL-4, IL-5, and IL-13) by 37.2%, 32.7%, and 34.0%, respectively, compared with the positive control. In contrast, splenic Th1 cytokine mRNA expression (IL-2, IL-12, and IFN-γ) was partially restored by 37.1%, 22.5%, and 18.7%, respectively. These findings indicate that BRB-F and BFR-F modulate multiple immune pathways and help restore Th1/Th2 immune balance, suggesting their potential as functional materials for regulating immune dysregulation associated with AD.

Background Atopic dermatitis (AD) is a chronic inflammatory skin disorder frequently associated with dysregulated Th1/Th2 immune balance and impaired regulatory T (Treg) activity. Although conventional treatments can reduce clinical symptoms, concerns regarding long-term adverse effects have led to increased interest in complementary and functional dietary materials with immunomodulatory potential. Bioprocessed black rice bran (BRB-F) and balloon flower root fractions (BFR-F) have individually demonstrated anti-inflammatory activities, but their combined oral efficacy and mechanisms in AD remain insufficiently characterized. Methods Mechanistic in vitro assays were first performed using a human B-cell line to measure IgE secretion, mouse and/or human mast cells to evaluate degranulation and TSLP release, and keratinocyte cultures to quantify TARC, MDC, and IL-6 production. These assays were used to determine whether BRB-F and BFR-F individually or cooperatively modulate immune and epithelial cell activation relevant to AD pathology. Subsequently, an AD-like phenotype was induced in BALB/c mice by topical application of 1-chloro-2,4-dinitrobenzene followed by mite extract. Animals received dietary supplementation with a 3:1 BRB-F:BFR-F mixture (10–80 mg/kg/day), and clinical skin inflammation, ear histopathology, and cytokine profiles were analyzed to assess Th1/Th2 balance and Treg-associated markers. Results Dietary supplementation with the BRB-F:BFR-F binary combination resulted in dose-dependent improvement in AD-like skin lesions and reduced histopathological severity. The mixture suppressed Th2 cytokines (IL-4, IL-5, IL-13) in ear tissue and increased splenic Th1 cytokines (IL-2, IL-12, IFN-γ), accompanied by dose-dependent elevation of galectin-9, suggesting activation of Treg-associated pathways. IL-10 expression was also reduced in vivo. In vitro, BRB-F and BFR-F cooperatively inhibited IgE production by B cells, attenuated mast cell activation and TSLP release, and lowered keratinocyte secretion of TARC, MDC, and IL-6. Conclusions The combined oral administration of bioprocessed BRB-F and BFR-F exerts multi-targeted anti-atopic activity that includes modulation of Th1/Th2 immune balance, activation of Treg-associated signaling, and suppression of B-cell, mast cell, and keratinocyte responses. These findings, confirmed by histopathology of skin tissues before and after treatment, provide preclinical support for the development of BRB-F:BFR-F as a complementary functional material for managing immune dysregulation associated with AD, although validation in human patients will be required.

Bisphenol A (BPA) is a representative obesogen that induces adipocyte differentiation and lipid accumulation by mimicking the action of hormones. Brassica juncea is a plant belonging to the mustard family, and has antioxidant, anti-inflammatory, and anti-obesity effects. However, its efficacy against obesogen-induced obesity requires further investigation. In this study, we investigated the anti-obesogenic effects of Brassica juncea extract (BJE) on BPA-treated 3T3-L1 preadipocytes and C57BL/6J mice. The treatment with BPA and BJE did not have cytotoxic effects in vitro. In addition, BJE inhibited BPA-induced lipid accumulation and suppressed BPA-induced changes in adipocyte differentiation, adipogenesis, and lipolysis protein expression in 3T3-L1 cells. Oral administration of BJE reduced body weight, adipose tissue mass, and adipocyte size in BPA-induced obese C57BL/6 mice. BJE also regulated the expression of proteins involved in adipocyte differentiation, adipogenesis, and lipolysis. These data demonstrate that BJE is a natural functional substance with anti-obesogenic effects.

Obesity is a global health concern. Recent research has suggested that the development of anti-obesity ingredients and functional foods should focus on natural products without side effects. We examined the effectiveness and underlying mechanisms of Brassica juncea extract (BJE) in combating obesity via experiments conducted in both in vitro and in vivo obesity models. In in vitro experiments conducted in a controlled environment, the application of BJE demonstrated the ability to suppress the accumulation of lipids induced by MDI in 3T3-L1 adipocytes. Additionally, it downregulated adipogenic-related proteins peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT/enhancer-binding protein-α (C/EBP-α), adipocyte protein 2 (aP2), and lipid synthesis-related protein acetyl-CoA carboxylase (ACC). It also upregulated the heat generation protein peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) and fatty acid oxidation protein carnitine palmitoyltransferase-1 (CPT-1). The oral administration of BJE decreased body weight, alleviated liver damage, and inhibited the accumulation of lipids in mice with diet-induced obesity resulting from a high-fat diet. The inhibition of lipid accumulation by BJE in vivo was associated with a decreased expression of adipogenic and lipid synthesis proteins and an increased expression of heat generation and fatty acid oxidation proteins. BJE administration improved obesity by decreasing adipogenesis and activating heat generation and fatty acid oxidation in 3T3-L1 cells and in HFD-induced obese C57BL/6J mice. These results suggest that BJE shows potential as a natural method for preventing metabolic diseases associated with obesity.

Obesity is a global health concern. Recent research has suggested that the development of anti-obesity ingredients and functional foods should focus on natural products without side effects. We investigated the anti-obesity efficacy and mechanisms of action of Brassica juncea extract (BJE) using in vitro and in vivo obesity models. In in vitro experiments, BJE treatment downregulated adipogenic-related proteins CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), adipocyte protein 2 (aP2), and lipid synthesis-related protein acetyl-CoA carboxylase (ACC). It also upregulated the heat generation protein peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) and fatty acid oxidation protein carnitine palmitoyltransferase-1 (CPT-1). Oral administration of BJE decreased body weight, alleviated liver damage, and inhibited lipid accumulation in high-fat diet (HFD)-induced obese mice. Inhibition of lipid accumulation by BJE in vivo was associated with decreased expression of adipogenic and lipid synthesis proteins and increased expression of heat generation and fatty acid oxidation proteins. BJE administration improved obesity by decreasing adipogenesis and activating heat generation and fatty acid oxidation in 3T3-L1 cells and in HFD-induced obese C57BL/6J mice. These findings indicate that BJE is a promising natural means of preventing obesity-related metabolic diseases.