Quercetin is a well-known antioxidant and a plant polyphenolic of flavonoid group found in many fruits, leaves, and vegetables. Propionibacterium acnes is a key skin pathogen involved in the progression of acne inflammation. Although quercetin has been applied to treat various inflammatory diseases, the effects of quercetin on P. acnes-induced skin inflammation have not been explored. This study investigated the effects of quercetin on P. acnes-induced inflammatory skin disease in vitro and in vivo. The results showed that quercetin suppressed the production of pro-inflammatory cytokines in P. acnes-stimulated HaCaT, THP-1 and RAW 264.7 cells. Additionally, quercetin reduced the production of TLR-2 and the phosphorylation of p38, ERK and JNK MAPKs in P. acnes-stimulated HaCaT and THP-1 cells. It also suppressed MMP-9 mRNA levels in two cell lines exposed to P. acnes in vitro. In the case of in vivo, P. acnes was intradermally injected into the ears of mice and it resulted in cutaneous erythema, swelling, and a granulomatous response. Treatment with quercetin markedly reduced ear thickness and swelling. These results suggested that quercetin can be a potential therapeutic agent against P. acnes-induced skin inflammation and may have diverse pharmaceutical and cosmetics applications.

To explore the role of Forsythoside I (FI) in acute lung injury (ALI) mouse and its underling mechanism.

The cell models of ALI are constructed by LPS induction. After pretreatment with different concentrations of FI, the lung injury is assessed by pathological changes of lung tissues and cell apoptosis. The cell viability, levels of pro-inflammatory cytokines, and the activation of TXNIP/NLRP3 pathway are inspected to investigate whether the effect of FI on inflammatory response is exerted by regulating the TXNIP/NLRP3 pathway.

LPS induces inflammatory cell infiltration, tissue necrosis and pulmonary interstitial edema of mouse tissues, and LPS increases the protein concentration and levels of pro-inflammatory factors in mouse BALF. Additionally, enhanced cell apoptotic level, increased W/D ratio and MPO activity, as well as suppressed SOD activity are observed in LPS-induced mouse models. Those inflammation response, oxidative stress and lung injury can be attenuated by FI (12.5 mg/kg, 25 mg/kg, 50 mg/kg) in a dose-dependent manner. Meanwhile, both in vitro and in vivo studies reveal that FI can lead to suppressed TXNIP expression and inactivated NLRP3 inflammasomes. TXNIP is an upstream target of NLRP3, and FI mitigates ALI by decreasing TXNIP to block NLRP3 inflammasomes.

FI protects against ALI through the mediation of TXNIP/NLRP3 inflammasome axis and therefore has a certain potential for ALI treatment.

FI protects against ALI through the mediation of TXNIP/NLRP3 inflammasome axis and therefore has a certain potential for ALI treatment.Interferon regulatory factor 7 (IRF7) is a crucial regulator of type I interferons (IFNs) against pathogen infections and plays a significant role in the endosomal Toll-like receptor signaling (namely, TLR7 and TLR9) in plasmacytoid dendritic cells (pDCs). In this study, we identify MEKK3, one of the MAP3K kinase, as a potent stimulator of IRF7 upon cellular activation of the TLR7/9 signaling pathways to induce various type I IFNs. The knockdown of MEKK3 in vivo substantially impairs type I IFN induction and increases susceptibility to HSV-1 infection in mice. Overexpression of MEKK3 significantly activates IRF7 to trigger strong induction of type I IFNs, while cells deficient in MEKK3 expression show abrogated innate immune responses to TLR7/TLR9 ligands stimulation. We confirmed that the IFNs’ induction is due to a MEKK3 and IRF7 interaction; it leads to the phosphorylation of IRF7 at multiple sites. Moreover, endogenous MEKK3 can bind and phosphorylate IRF7 after TLR9 activation by its specific ligand CpG DNA. It is the first time to report the role of MEKK3 on type I IFN, which indicates crosstalk between MAP3K activation and type I IFNs’ induction in the endosomal Toll-like receptor pathways.Degradation of polysaccharides to afford low-molecular-weight oligosaccharides have been shown to produce new bioactivities that are not present in the starting material. The simplicity of ultrasonic treatment in the degradation of a polysaccharide, such as κ-carrageenan, offers practical advantage in producing degraded products with lower molecular weight that may have new interesting potential activities. This study embarked on investigating the effects in molecular weights and structural changes of κ-carrageenan under varying ultrasonic conditions. Molecular weight (MW) monitoring of ultrasonically-treated κ-carrageenan at various conditions were done by gel permeation chromatography. The product formed using the optimized condition was characterized using FTIR and NMR. The decrease in MW has been shown to be dependent on low concentration (5.0 mg mL-1), high amplitude (85%), and long treatment time (180 mins) to afford a degraded κ-carrageenan with average molecular weight (AMW) of 41,864 Da, which is a 96.33% reduction from the raw sample with initial AMW of 1,139,927 Da. Structural analysis reveals that most of the peaks of the raw κ-carrageenan was retained with minor change. 1D and 2D NMR analyses showed that the sonic process afforded a product where the sulfate group at the G4S-4 position was cleaved forming a methylene in the G4S ring. The results would be useful in the structure-activity relationship of κ-carrageenan oligosaccharides and in understanding the effect in the various potential applications of degraded κ-carrageenan.A sound driven air bubble can be transformed into an argon bubble emitting light pulses stably. The very foundation to investigate the sonoluminescing bubble is to accurately determine the ambient radius and gas composition in the interior. The conventional approach is to model the air-to-argon transformation process through a large number of bubble dynamics simulations to obtain the physical parameters of the ultimate argon bubble. In this paper, we propose a highly efficient method to pinpoint this information in a phase diagram. The method is based on the diffusive equilibrium for each species inside the bubble and derives the ambient radius and composition inversely. To calculate the former parameter, the bisection algorithm is employed to consecutively narrow down the searching range until the equilibria is approached. Afterward, several cycles of full dynamics simulations are conducted to refine the composition. The method is validated using published experimental data. Colforsin activator The calculated ambient radii deviate from the test results by less than 1 μm, which falls within the margin of measurement error.