Pistacia lentiscus L. Distilled Leaves as a Potential Cosmeceutical Ingredient: Phytochemical Characterization, Transdermal Diffusion, and Anti-Elastase and Anti-Tyrosinase Activities

The present work was performed to investigate the phenolic composition of P. lentiscus L. distilled leaves (PDL) and examine its potential against certain key enzymes related to skin aging.
High-pressure liquid chromatography coupled to mass spectrometry (HPLC-MS) and various separation procedures combined with nuclear magnetic resonance (NMR) and MS analysis were performed to isolate and identify compounds present in the ethyl acetate extract (EAE) of PDL.
A high amount of flavonol glycoside was detected in EAE.
Indeed, quercetin-3-O-rhamnoside (FC), myricetin-3-O-rhamnoside (FM2), and kaempferol-3-O-rhamnoside (FB2) were isolated from EAE, and are present in high quantities of 10.47 ± 0.26, 12.17 ± 0.74, and 4.53 ± 0.59 mg/g dry weight, respectively. A transdermal diffusion study was carried out to determine the EAE-molecules that may transmit the cutaneous barrier and showed that FM2 transmits the membrane barrier with a high amount followed by FC. EAE, FM2, and FC were tested against tyrosinase and elastase enzymes.
Moreover, intracellular tyrosinase inhibition and cytotoxicity on skin melanoma cells (B16) were evaluated.
The results indicated that EAE, FC, and FM2 have important inhibitory activities compared to the well-known standards, at non-cytotoxic concentrations. Therefore, they could be excellent agents for treating skin pigmentation and elasticity problems.

Molecular Analysis of the Contribution of Alkaline Protease A and Elastase B to the Virulence of Pseudomonas aeruginosa Bloodstream Infections

Pseudomonas aeruginosa is a major cause of nosocomial bloodstream infections.
This microorganism secretes two major proteases, alkaline protease A (AprA) and elastase B (LasB). Despite several in vitro studies having demonstrated that both purified proteases cleave a number of components of the immune system, their contribution to P. aeruginosa bloodstream infections in vivo remains poorly investigated.
In this study, we used a set of isogenic mutants deficient in AprA, LasB or both to demonstrate that these exoproteases are sufficient to cleave the complement component C3, either soluble or deposited on the bacteria.
Nonetheless, exoprotease-deficient mutants were as virulent as the wild-type strain in a murine model of systemic infection, in Caenorhabditis elegans and in Galleria mellonella.
Consistently, the effect of the exoproteases on the opsonization of P. aeruginosa by C3 became evident four hours after the initial interaction of the complement with the microorganism and was not crucial to survival in blood. These results indicate that exoproteases AprA and LasB, although conferring the capacity to cleave C3, are not essential for the virulence of P. aeruginosa bloodstream infections.

Engineering Molecular Probes for In Vivo Near-Infrared Fluorescence/Photoacoustic Duplex Imaging of Human Neutrophil Elastase

Early detection of human neutrophil elastase (HNE), the potential biomarker of lung cancer, is crucial for the accurate diagnosis and evaluation of lung cancer.
Currently, little progress of HNE-activated probes has been made for in vivo imaging. Herein, assisted by probe-active pocket match engineering, we synthesized a series of near-infrared fluorescence (NIRF) and photoacoustic (PA) duplex imaging probes by conjugating diverse fluorinated amide chains onto hemi-cyanine.
Finally, we identified that probe 2 (denoted as LET-8), with the pentafluoroethyl group, is a superior probe to detect HNE with the best selectivity as well as good response ability and thus successfully realized NIRF/PA duplex imaging of HNE activity both in vitro and in vivo.

Suppressive effects of the neutrophil elastase inhibitor sivelestat sodium hydrate on interleukin-1β production in lipopolysaccharide-stimulated porcine whole blood

Objective: Sivelestat sodium hydrate (Siv) is expected to be an effective therapy for acute respiratory distress syndrome, although its mechanism of action is not understood. In this study, we investigated which myeloid cells-derived cytokines were suppressed by Siv.
Methods: Continuous hemofiltration was performed by circulating fresh porcine blood through a semi-closed circuit. To ensure that leukocytes survived for 360 min, 5% glucose, heparin, and air were continuously injected. The control group received continuous administration of lipopolysaccharide (LPS) only, whereas the Siv group received LPS and Siv. Complete blood count, levels of various cytokines, and other variables were compared between the groups.
Results: Interleukin (IL)-1β level was significantly suppressed in the Siv group compared with that in the control group (p<0.05).
Conclusions: The results suggested that Siv suppressed the production of IL-1β and possibly other cytokines by myeloid cells. Whether this suppression of cytokine production is caused directly by Siv or mediated via suppression of granulocyte elastase should be evaluated in the future.
Keywords: Acute respiratory distress syndrome; Cytokine; Myeloid cell; Sivelestat sodium hydrate.

Protective effects of neuropeptide Y against elastase-induced pulmonary emphysema

Neuropeptide Y (NPY) is a neuropeptide widely expressed in not only the central nervous system but also immune cells and the respiratory epithelium. Patients with chronic obstructive pulmonary disease (COPD) reportedly exhibit decreased NPY expression in the airway epithelium, but the involvement of NPY in the pathophysiology of COPD has not been defined.
We investigated the role of NPY in elastase-induced emphysema. NPY-deficient (NPY-/-) mice and wild-type (NPY+/+) mice received intratracheal instillation of porcine pancreas elastase (PPE). The numbers of inflammatory cells and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates were determined along with quantitative morphometry of lung sections. Intratracheal instillation of PPE induced emphysematous changes and increased NPY levels in the lungs.
Compared with NPY+/+ mice, NPY-/- mice had significantly enhanced PPE-induced emphysematous changes and alveolar enlargement. Neutrophilia seen in BAL flu12id of NPY+/+ mice on day 4 after PPE instillation was also enhanced in NPY-/- mice, and the enhancement was associated with increased levels of neutrophil-related and macrophage-related chemokines and IL-17A as well as increased numbers of type 3 innate lymphoid cells in the airways. Treatment with NPY significantly reduced PPE-induced emphysematous changes.
Conversely, treatment with a NPY receptor antagonist exacerbated PPE-induced emphysematous changes.
These observations indicate that NPY has protective effects against elastase-induced emphysema, and suggest that targeting NPY in emphysema has potential as a therapeutic strategy for delaying disease progression.

µCT to quantify muco-obstructive lung disease and effects of neutrophil elastase knockout in mice

Muco-obstructive lung diseases are characterized by airway obstruction and hyperinflation, which can be quantified by imaging.
Our aim was to evaluate µCT for longitudinal quantification of muco-obstructive lung disease in β-epithelial Na+ channel overexpressing (Scnn1b-TG) mice and of the effects of neutrophil elastase (NE) knockout on its progression.
Lungs from wild-type (WT), NE-/-, Scnn1b-TG, and Scnn1b-TG/NE-/- mice were scanned with 9 µm resolution at 0, 5, 14 and 60 days of age, and airway and parenchymal disease was quantified. Mucus adhesion lesions (MAL) were persistently increased in Scnn1b-TG compared to WT mice from 0 days (20.25±6.50 vs. 9.60±2.07, P<0.05), and this effect was attenuated in Scnn1b-TG/NE-/- mice (5.33±3.67, P<0.001). Airway wall area percentage (WA%) was increased in Scnn1b-TG mice compared to WT from 14 days onward (59.2±6.3% vs. 49.8±9.0%, P<0.001) but was similar in Scnn1b-TG/NE-/- compared to WT at 60 days (46.4±9.2% vs. 45.4±11.5%, P=0.97).

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Air proportion (Air%) and mean linear intercept (Lm) were persistently increased in Scnn1b-TG compared to WT from 5 days on (53.9±4.5% vs. 30.0±5.5% and 78.82±8.44µm vs. 65.66±4.15µm, respectively, P<0.001), whereas in Scnn1b-TG/NE-/- Air% and Lm were similar to WT from birth (27.7±5.5% vs.27.2±5.9%, P =0.92 and 61.48±9.20µm vs. 61.70±6.73µm, P=0.93, respectively).
Our results suggest that µCT is sensitive to detect the onset and progression of muco-obstructive lung disease and effects of genetic deletion of NE on the morphology of airways and lung parenchyma in Scnn1b-TG mice, and that it may serve as a sensitive endpoint for preclinical studies of novel therapeutic interventions for muco-obstructive lung diseases.

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