Atopic dermatitis (AD) is a chronic inflammatory skin disease stemming from genetic susceptibility and environmental factors. It is characterized by immune dysregulation, increased mast cell activity, elevated levels of immunoglobulin E (IgE), and excessive proinflammatory mediator expression. These factors contribute to hallmark symptoms such as pruritus, erythema, and skin barrier dysfunction. In this study, we investigated the antioxidant and anti-inflammatory effects of Taraxacum mongolicum (WTM) water extract, as well as its skin barrier regulation and immune functions in AD. In the present study, we explored the therapeutic efficacy and underlying mechanisms of WTM in a BALB/c mouse model of AD induced by 2,4-dinitrochlorobenzene (DNCB). Mice were administered WTM orally or topically for 14 consecutive days. The results demonstrated that WTM treatment significantly alleviated clinical severity, showing reductions in skin lesion scores, epidermal thickness, mast cell infiltration, and scratching behavior, compared to the DNCB-treated group. Mechanistically, WTM reduced serum levels of IgE and proinflammatory cytokines (IL-4, IL-6, IL-1β, TNF-α, and IL-31) while suppressing the expression of the JAK/STAT/TSLP signaling pathway in skin tissues. Furthermore, WTM inhibited the TLR4/NF-κB and MAPK pathways and enhanced antioxidant defense by elevating superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activities. These findings indicate that WTM attenuates DNCB-induced AD progression in mice, likely through the dual modulation of inflammatory signaling and oxidative stress. These findings suggest that WTM may modulate the immune response and alleviate AD symptoms by inhibiting the TLR4/NF-κB, MAPK, and JAK/STAT/TSLP pathways.

Momordica charantia L. (MC), also referred to as bitter gourd or bitter melon, is a Cucurbi taceae plant renowned for its medicinal benefits. 5-Fluorouracil (5-FU) is employed as a frontline chemotherapeutic agent, with its antitumor activity mediated through the inhibition of DNA and RNA synthesis. However, its therapeutic efficacy is often compromised by serious adverse effects, particularly gastrointestinal inflammation. Therefore, this research examined the efficacy of the ethanolic extract of Momordica charantia fruit (EMC) in mitigating 5-FU-induced intestinal mucositis in mice. Mucositis was induced in mice by intraperitoneal administration of 5-FU at 50 mg/kg from experimental days 4 to 7, with EMC administered orally at doses of 125 mg/kg and 250 mg/kg once daily for ten consecutive days. 5-FU exposure resulted in severe intestinal injury, manifested by markedly upregulated inflammation and oxidative stress. EMC treatment significantly reversed these pathophysiological alterations, restoring mucosal architecture and function. Furthermore, EMC effectively reduced the 5-FU-induced release of inflammatory mediators and oxidative stress markers. These results demonstrate that EMC acts as a novel protective modulator of 5-FU-induced mucositis, offering substantial translational potential as an adjunctive supportive therapy in colorectal cancer management.

The emergence of SARS-CoV-2, the etiological agent of COVID-19, has resulted in widespread global infection and millions of deaths. Viral entry is initiated by the interaction between the viral spike (S) protein and the host cell receptor ACE2, followed by TMPRSS2-mediated proteolytic activation that facilitates membrane fusion. Bitter melon (Momordica charantia L., MC), a traditional medicinal and edible plant widely used in tropical Asia, possesses notable anti-inflammatory, antioxidant, antitumor, and hypoglycemic properties. In this study, the ethanol extract of bitter melon (EMC) markedly downregulated ACE2 and TMPRSS2 expression in both in vitro and in vivo models without inducing cytotoxicity. Furthermore, phytochemicals isolated from EMC—including p-coumaric acid, rutin, and quercetin—exhibited comparable inhibitory effects. These results indicate that EMC and its bioactive constituents may interfere with SARS-CoV-2 entry by modulating the ACE2/TMPRSS2 axis, highlighting their potential as natural adjuncts for COVID-19 prevention or management.

Angiotensin-converting enzyme 2 (ACE2) is a cell-surface receptor that helps the body regulate blood pressure and endocrine secretions. Transmembrane serine protease 2 (TMPRSS2) is a cell surface protein expressed mainly by endothelial cells of the respiratory and digestive tract, which participates in the cleavage of protein peptide bonds with serine as the active site. These two proteins have been studied to be highly associated with infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Soybean trypsin inhibitor (SBTI) has special bioactivities such as anticarcinogenic and anti-inflammatory functions, which can be widely used in functional foods or drugs. Our study involved in vitro and in vivo experiments to elucidate the effect of SBTI on SARS-CoV-2 host invasion. First, it was confirmed that being under 250 μg/mL of SBTI was not toxic to HepG2, HEK293T, and Calu-3 cells. The animal study administered SBTI to mice once daily for 14 days. In the lungs, liver, and kidneys, the histopathologic findings of the SBTI group were not different from those of the control group, but the expression of ACE2, TMPRSS2, and CD147 was reduced. Thus, our findings suggest that the inhibition of ACE2, TMPRSS,2 and CD147 proteins by SBTI shows promise in potentially inhibiting SARS-CoV-2 infection.

5-Fluorouracil (5-FU) remains a cornerstone chemotherapeutic for colorectal cancer, exerting its antitumor effects primarily through disruption of DNA and RNA synthesis and subsequent induction of apoptosis. Nonetheless, its clinical efficacy is often compromised by prominent adverse effects, particularly mucositis. This study examines the potential of brown-strain Flammulina velutipes Singer (FVB) to alleviate 5-FU-associated intestinal damage in a mouse model, offering insights into its possible role in mitigating chemotherapy-induced toxicity. 5-FU treatment significantly exacerbated gastrointestinal toxicity, as evidenced by severe diarrhea, shortened colon length, villus atrophy, and architectural disorganization of the intestine. It also inhibited crypt cell proliferation and induced body weight loss. Mechanistically, 5-FU activated pro-inflammatory, apoptotic, oxidative stress, and EMT pathways and disrupted mucosal tight junctions. Notably, FVB administration mitigated these pathological changes, indicating its protective role against 5-FU-induced intestinal injury. In summary, this investigation presents novel evidence for the protective role of FVB in mitigating 5-FU-induced intestinal mucositis. The results highlight the therapeutic potential of FVB as an adjunct to chemotherapy, potentially reducing treatment-related toxicity and enhancing the clinical care and quality of life of individuals undergoing colorectal cancer therapy.