Treatment Effect of Phototherapy with Low-Level Energy in Patients with Allergic Rhinitis: A Single-Arm Observational Study.

Allergic rhinitis is one of the most common health challenges and has a chronic and repetitive course that requires symptomatic treatment. We aimed to investigate the effect of phototherapy on allergic rhinitis and how long it takes to demonstrate treatment effect. Twenty-one patients who were diagnosed with allergic rhinitis using the skin prick test were enrolled. Red light (660 nm) and infrared light (940 nm) with a low power energy of 5 mW were used three times a day at intervals of at least 5 h. The Rhinoconjuntivitis Quality of Life Questionnaire (RQLQ) and a visual analog scale (VAS) were used to measure the changes in symptoms. The median RQLQ and VAS scores before treatment were 62 (49-81.5) and 3 (2-5) points, respectively. The RQLQ score improved significantly at two and four weeks after treatment (52 [39-62.5]) and 46.0 [30.5-57.0], respectively). The VAS scores also improved significantly at two and four weeks after treatment. Nasal obstruction and rhinorrhea improved significantly at one week after the procedure. Low-power (5 mW) light irradiation (660 nm red light and 940 nm infrared) was effective in improving the symptoms of allergic rhinitis. In addition, symptom improvement became clear approximately a week after use. Further studies are required to reach a definitive conclusion.

A Comparative Study on Photo-Protective and Anti-Melanogenic Properties of Different Kadsura coccinea Extracts.

Kadsura coccinea (KC), a beneficial plant for human health, has been used for centuries in China, Thailand, and Korea in folk medicine and food. There is evidence supporting the biological effects of highly bioactive ingredients in KC such as lignans, triterpenoids, flavonoids, phenolic acids, steroids, and amino acids. In this study, we aimed to explore the effects, functions, and mechanisms of the extracts from KC root (KCR), stem (KCS), leaf (KCL), and fruit (KCF) in UVA and UVB-irradiated keratinocytes and α-melanocyte stimulating hormone (α-MSH)-stimulated melanocytes. First, the total polyphenol and flavonoid contents of KCR, KCS, KCL, and KCF and their radical scavenging activities were investigated. These parameters were found to be in the following order: KCL > KCR > KCS > KCF. UVA and UVB-irradiated keratinocytes were treated with KCR, KCS, KCL, and KCF, and keratinocyte viability, LDH release, intracellular ROS production, and apoptosis were examined. Our results demonstrated that KC extracts improved keratinocyte viability and reduced LDH release, intracellular ROS production, and apoptosis in the presence UVA and UVB irradiation. The overall photoprotective activity of the KC extracts was confirmed in the following order: KCL > KCR > KCS > KCF. Moreover, KC extracts significantly decreased the intracellular melanin content and tyrosinase activity in α-MSH-stimulated melanocytes. Mechanistically, KC extracts reduced the protein and mRNA expression levels of tyrosinase, tyrosinase-related protein-1 (TRP-1), and tyrosinase-related protein-2 (TRP-2) in α-MSH-stimulated melanocytes. In addition, these extracts markedly downregulated myophthalmosis-related transcription factor expression and cAMP-related binding protein phosphorylation, which is upstream of the regulation of Tyrosinase, TRP-1, and TRP-2. The overall anti-melanogenic activity of the KC extracts was established in the following order. KCL > KCR > KCS > KCF. Overall, the KC extracts exert photoprotective and anti-melanogenic effects, providing a basis for developing potential skin-whitening and photoprotective agents.

Costunolide inhibits osteoclast differentiation by suppressing c-Fos transcriptional activity.

Costunolide, a sesquiterpene lactone, exhibits anti-inflammatory and anti-oxidant properties and mediates apoptosis. However, its effects and mechanism of action in osteoclasts remain unknown. Herein, we found that costunolide significantly inhibited RANKL-induced BMM differentiation into osteoclasts in a dose-dependent manner without affecting cytotoxicity. Costunolide did not regulate the early signaling pathways of RANKL, including the mitogen-activated protein kinase and NF-κB pathways. However, costunolide suppressed nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) expression via inhibition of c-Fos transcriptional activity without affecting RANKL-induced c-Fos expression. The inhibitory effects of costunolide were rescued by overexpression of constitutively active (CA)-NFATc1. Taken together, our results suggest that costunolide inhibited RANKL-induced osteoclast differentiation by suppressing RANKL-mediated c-Fos transcriptional activity.