Atopic dermatitis (AD, eczema) is a condition that causes dry, itchy, and inflamed skin and occurs most frequently in children but also affects adults. However, common clinical treatments provide limited relief and have some side effects. Therefore, there is a need to develop new effective therapies to treat AD. Epi-oxyzoanthamine is a small molecule alkaloid isolated from Formosan zoanthid. Relevant studies have shown that zoanthamine alkaloids have many pharmacological and biological activities, including anti-lymphangiogenic functions. However, there are no studies on the use of epi-oxyzoanthamine on the skin. In this paper, epi-oxyzoanthamine has been shown to have potential in the treatment of atopic dermatitis. Through in vitro studies, it was found that epi-oxyzoanthamine inhibited the expression of cytokines in TNF-α/IFN-γ-stimulated human keratinocyte (HaCaT) cells, and it reduced the phosphorylation of MAPK and the NF-κB signaling pathway. Atopic dermatitis-like skin inflammation was induced in a mouse model using 2,4-dinitrochlorobenzene (DNCB) in vivo. The results showed that epi-oxyzoanthamine significantly decreased skin barrier damage, scratching responses, and epidermal hyperplasia induced by DNCB. It significantly reduced transepidermal water loss (TEWL), erythema, ear thickness, and spleen weight, while also increasing surface skin hydration. These results indicate that epi-oxyzoanthamine from zoanthid has good potential as an alternative medicine for treating atopic dermatitis or other skin-related inflammatory diseases.

DRG adhesion is a key pathological feature of failed back surgery syndrome and a major cause of neuropathic pain. DRG, or epidural adhesion, commonly results from spinal surgery, leakage of disk material into the epidural space, or inflammation. To better mimic this clinical condition, we developed a novel and reliable animal model of DRG adhesion-induced neuropathic pain. Using this model, we investigated the therapeutic potential and underlying mechanisms of CLARIX FLO, a sterile, particulate human amniotic membrane and umbilical cord tissue product. Our results demonstrate that CLARIX FLO exerts significant analgesic and anti-inflammatory effects in the DRG adhesion model. The application of CLARIX FLO to the injured DRG markedly attenuated mechanical allodynia. CLARIX FLO treatment also reduced outer sheath thickening, suppressed the inflammatory microenvironment, and decreased hypersensitivity of isolectin B4-positive neurons. Mechanistically, CD44 was identified as a potential downstream mediator of CLARIX FLO. Furthermore, a high dose of HC-HA/PTX3, the key bioactive component of CLARIX FLO, effectively reversed mechanical allodynia and inflammation. Notably, CLARIX FLO inhibited the overexpression of TNF-α and TRPV1 adhering to the DRG. In this study, we demonstrated that CLARIX FLO effectively alleviates DRG adhesion-induced neuropathic pain through a CD44–TRPV1-dependent mechanism.

Background and Objectives: Postoperative pain after endoscopic discectomy may reflect acute surgical nociception superimposed on pre-existing radicular symptoms. Molecular hydrogen (H₂) has antioxidant and anti-inflammatory properties, but clinical evidence for perioperative analgesia is limited. We evaluated the association between perioperative H₂ inhalation and postoperative pain and analgesic requirements. Materials and Methods: This open-label, non-randomized pilot study enrolled 37 patients in two consecutive periods (H₂, n = 25; control, n = 12). Because original outcome records for 12 H₂-period participants could no longer be retrieved at the time of manuscript preparation, the complete-case clinical analysis included 25 source-verifiable participants (H₂, n = 13; control, n = 12). H₂ was delivered via nasal cannula as a 66.7% H₂/33.3% O₂ source gas at 2 L/min (estimated inspired H₂ approximately 4%). Pain was evaluated with a numerical rating scale (NRS) preoperatively, at post-anesthesia care unit (PACU) arrival, at 1, 6, 12, and 24 h, and at 1 month. Longitudinal scores were analyzed using generalized estimating equations with Holm-adjusted comparisons. A parallel exploratory murine chronic constriction injury (CCI) experiment (n = 6/group) assessed mechanical allodynia over 14 days of daily H₂ inhalation. Results: The group-by-time interaction was significant (Wald χ²(6) = 56.68, p < 0.001). After Holm adjustment, pain scores were lower with H₂ at PACU arrival (difference, −3.21; adjusted p = 0.002), 1 h (−2.42; adjusted p = 0.004), and 1 month (−3.45; adjusted p < 0.001). Intraoperative fentanyl use and rescue analgesic use were also lower in the H₂ group; no adverse events were documented in the analyzed cohort. In the murine CCI experiment, H₂-treated mice showed higher ipsilateral paw withdrawal thresholds than air-exposed controls. Conclusions: Perioperative H₂ inhalation was associated with lower pain scores at selected time points and reduced analgesic requirements. These preliminary findings require confirmation in randomized trials. Trial registration: ClinicalTrials.gov NCT05476575.

Background: Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss and is strongly driven by oxidative stress and inflammation. This study investigated the protective effects of cynarin against sodium iodate (NaIO₃)-induced retinal pigment epithelium (RPE) injury, focusing on the MAPK and NF-κB signaling pathways. Materials and Methods: Human ARPE-19 cells were exposed to NaIO₃, and cell viability was assessed by the MTT assay. Protein expression of MAPK components (p38, JNK, ERK) and the NF-κB pathway was analyzed by Western blotting, and pro-inflammatory cytokine (IL-1β, IL-6, TNF-α) mRNA expression was measured by RT-qPCR. In vivo, NaIO₃-induced retinal degeneration in C57BL/6 mice was treated with cynarin (3 or 10 mg/kg) for seven days, and retinal changes were evaluated by fundus photography, fluorescein angiography, and OCT. Results: Cynarin preserved ARPE-19 cell viability without cytotoxicity. It significantly attenuated NaIO₃-induced p38 and JNK phosphorylation, IκB degradation, and NF-κB activation while downregulating IL-1β, IL-6, and TNF-α expression. In vivo, cynarin reduced drusen-like lesions, hyperfluorescent abnormalities, and retinal thinning, and dose-dependently suppressed ocular pro-inflammatory cytokines. Conclusions: Cynarin protects against oxidative stress-induced retinal degeneration by suppressing MAPK and NF-κB inflammatory signaling, representing a promising therapeutic candidate for preventing or delaying NaIO₃-induced dry AMD-like retinal injury.